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Chinese Journal of Anesthesiology ; (12): 1252-1255, 2021.
Article in Chinese | WPRIM | ID: wpr-911353

ABSTRACT

Objective:To evaluate the role of histone deacetylase 3 (HDAC3) in high glucose hypoxia/reoxygenation (H/R) injury to primary rat cardiomyocytes and the relationship with autophagy.Methods:The primary cardiomyocytes extracted from newborn Sprague-Dawley rats, aged about 1-3 days, were divided into 5 groups ( n=24 each) according to the random number table method: control group (C group, glucose concentration 5.5 mmol/L), H/R group, high glucose group (H group, glucose concentration 30 mmol/L), high glucose H/R group (HH/R group), and high glucose H/R + HDAC3 inhibitor RGFP966 group (HH/R+ RG group). Fifty percent glucose injection was used to prepare high-glucose medium (final concentration 30 mmol/L). Cells were cultured in a hypoxic environment (5% CO 2-0.9% O 2-94.1% N 2) for 6 h, followed by reoxygenation in a normoxic environment for 2 h to establish the cardiomyocyte H/R model in H/R group.RGFP966 at a final concentration of 10 μmol/L was added at 24 h before H/R in HH/R+ RG group.At 2 h of reoxygenation, the cell viability was measured using CCK-8 kit, the activity of lactic dehydrogenase (LDH) in the cell supernatant was determined using enzyme-linked immunosorbent assay, the level of autophagy was detected with a confocal microscope after cells were transfected with autophagy double-labeled adenovirus (mRFP-GFP-LC3), and the expression of HDAC3, p62, LC3 Ⅱ and LC3 Ⅰ was detected using Western blot.LC3Ⅱ/LC3Ⅰ ratio was calculated. Results:Compared with group C, the cell viability was significantly decreased, and the activity of LDH in supernatant was increased in H/R and H groups, the number of autophagosomes was significantly increased, the expression of HDAC3 in cardiomyocytes was up-regulated, the expression of p62 was down-regulated, and the LC3 Ⅱ/I ratio was increased in group H/R, and the number of autophagosomes was significantly decreased, the expression of HDAC3 and p62 in cardiomyocytes was up-regulated, and the LC3 Ⅱ/I ratio was decreased in group H ( P<0.05). Compared with group H/R, the cell viability was significantly decreased, the activity of LDH in supernatant was increased, the number of autophagosomes was decreased, the expression of HDAC3 and p62 in cardiomyocytes was up-regulated, and the LC3 Ⅱ/I ratio was decreased in group HH/R ( P<0.05). Compared with group H, the cell viability was significantly decreased, the activity of LDH in supernatant was increased, the number of autophagosomes was increased, the expression of HDAC3 and p62 in cardiomyocytes was up-regulated, and the LC3 Ⅱ/I ratio was increased in group HH/R ( P<0.05). Compared with group HH/R, the cell viability was significantly increased, the activity of LDH in supernatant was decreased, the number of autophagosomes was increased, the expression of HDAC3 and p62 in cardiomyocytes was down-regulated, and the LC3 Ⅱ/I ratio was increased in group HH/R+ RG ( P<0.05). Conclusion:Up-regulation of HDAC3 expression is involved in high glucose H/R injury to primary rat cardiomyocytes, which is related to decreasing the level of autophagy.

2.
Article in Chinese | WPRIM | ID: wpr-911316

ABSTRACT

Objective:To evaluate the effect of TBK1 overexpression on hypoxia-reoxygenation (H/R) injury in isolated mouse cardiomyocytes subjected to high glucose and the relationship with mitochondrial autophagy.Methods:Normally cultured log-phase HL-1 mouse cardiomyocytes were inoculated in a 6-well plate at a density of 1×10 6 cells/ml and were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), high glucose group (group HG), high glucose and H/R group (group HG+ H/R), and TBK1 overexpression group (group TBK1). The cells were incubated in culture medium with 1% fetal bovine serum and 1% double antibody for 24 h when the cell density reached 50%.When the cell density reached 80%, pcDNA3.1 (+ ) was used as a vector to achieve TBK1 overexpression.The cells were cultured with high glucose medium (33 mmol/L) for 24 h, exposed to 94% N 2+ 5% CO 2+ 1% O 2 for 24 h in an incubator at 37℃ followed by 12 h reoxygenation in an incubator containing 5% CO 2 at 37°C to establish the model of H/R injury to cardiomyocytes subjected to high glucose.After reoxygenation, CCK-8 assay was used to detect cell viability, the activity of lactic dehydrogenase (LDH) in supernatant was detected using LDH kit, mitochondrial contents were determined using Mito-Tracter green fluorescent probe, and the expression of TBK1 and mitophagy-related proteins PINK1, Parkin, LC3B and P62 was detected by Western blot. Results:Compared with group C, the cell viability was significantly decreased, the activity of LDH in supernatant was increased, mitochondrial contents were decreased, the expression of TBK1, PINK1, Parkin and LC3B was down-regulated, and the expression of P62 was up-regulated in HG group and HG+ H/R group ( P<0.05). Compared with group HG, the cell viability was significantly decreased, the activity of LDH in supernatant was increased, mitochondrial contents were decreased, the expression of TBK1, PINK1, Parkin and LC3B was down-regulated, and the expression of P62 was up-regulated in group HG+ H/R ( P<0.05). Compared with group HG+ H/R, the the cell viability was significantly increased, the activity of LDH in supernatant was decreased, mitochondrial contents were increased, the expression of TBK1, PINK1, Parkin and LC3B was up-regulated, and the expression of P62 was down-regulated in group TBK1 ( P<0.05). Conclusion:The mechanism by which TBK1 overexpression reduces the H/R injury is related to restoring mitophagy in isolated mouse cardiomyocytes subjected to high glucose.

3.
Article in Chinese | WPRIM | ID: wpr-911248

ABSTRACT

Objective:To evaluate the effect of sirtuin 3 (SIRT3) overexpression on hypoxia-reoxygenation (H/R) injury to hippocampal neurons of mice exposed to high glucose and its relationship with SOD2.Methods:The normally cultured HT22 neurons at the logarithmic phase were selected and divided into 3 groups ( n=12 each) using a random number table method: high-glucose normoxia group (HG group), high glucose+ H/R group (HHR group) and high glucose+ H/R+ SIRT3 overexpression group (HHR+ SIRT3 group). To establish high glucose model, the neurons in 3 groups were cultured in high-glucose culture medium (glucose concentration of 50 mmol/L) for 8 h. In HHR and HHR+ SIRT3 groups, the cells were exposed to glucose-free and hypoxia for 6 h and then cultured in the high-glucose normoxic environment for 24 h to establish the high glucose and HR injury model.In HHR+ SIRT3 group, the neurons were transfected with SIRT3 overexpressed lentivirus.The cell viability was recorded by the cell counting kit-8 assay, reactive oxygen species (ROS) content was detected by flow cytometry, mitochondrial malonaldehyde (MDA) content, superoxide dismutase (SOD) activity, catalase (CAT) activity and adenosine triphosphate (ATP) content were determined by colorimetry, mitochondrial membrane potential (MMP) was detected by JC-1 probe, and the expression of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), SIRT3, SOD2 and acetylated SOD2 (ac-SOD2) was detected by Western blot. Results:Compared with HG group, cell viability, SOD activity, CAT activity, ATP content, MMP, NRF1 and the expression of TFAM and SIRT3 were significantly decreased, and ROS content, MDA content and ac-SOD2/SOD2 ratio were increased in group HHR and group HHR+ SIRT3 ( P<0.05). Compared with HHR group, cell viability, SOD activity, CAT activity, ATP content, MMP, NRF1 and the expression of TFAM and SIRT3 were significantly increased, and ROS content, MDA content and ac-SOD2 /SOD2 ratio were decreased in HHR+ SIRT3 group ( P<0.05). Conclusion:SIRT3 overexpression can alleviate hypoxia-reoxygenation (H/R) injury to hippocampal neurons of mice incubated in high glucose medium, and the mechanism is related to activation of SOD2 deacetylation.

4.
Article in Chinese | WPRIM | ID: wpr-911242

ABSTRACT

Objective:To evaluate the role of hypoxia-inducible factor-1α (HIF-1α) in the renal injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats and its relationship with solute carrier family7 member11 (SLC7A11).Methods:SPF-grade healthy male Sprague-Dawley rats, aged 4 weeks, weighing 100-130 g, were fed with high-fat and high-sucrose diet freely.The weight of the rats was measured once a week.After the weight of the animals reached 240 g, 1% streptozotocin (STZ)-citrate buffer 35 mg/kg was injected intraperitoneally to induce type 2 diabetes mellitus.After injection of STZ, the animals were fed with high-fat and high-sucrose diet continuously.Blood samples were collected from the tail vein for determination of blood glucose concentrations 1 week later.When random blood glucose was ≥16.7 mmol/L for 3 times, the model of type 2 diabetes mellitus was considered to be established successfully.After the model was established successfully, the animals were fed with high-fat and high-sucrose diet continuously for 6 weeks.Eighteen rats with type 2 diabetes mellitus were selected and divided into 3 groups ( n=6 each) using a random number table method: diabetic sham operation group (group DS), diabetic myocardial I/R group (group DIR) and diabetic myocardial I/R+ HIF-1α agonist DMOG group (DIR+ DMOG group). Twelve non-diabetic rats were divided into 2 groups ( n=6 each) using a random number table method: non-diabetic sham operation group (NS group) and non-diabetic myocardial I/R group (NIR group). The rat myocardial I/R injury model was established by ligating the anterior descending branch of the left coronary artery for 30 min followed by 120 min reperfusion in anesthetized rats.Blood samples were collected from the right internal carotid artery at 120 min of reperfusion for determination of the serum creatinine (Cr), urea nitrogen (BUN) and neutrophil gelatinase-associated lipocalin (NGAL) concentrations (by enzyme-linked immunosorbent assay). Renal tissues were obtained for examination of the pathological changes (by HE staining method) and for determination of the expression of HIF-1α and SLC7A11 (by Western blot). The damage to the renal tubules was scored. Results:Compared with group NS, the concentrations of serum Cr, BUN and NGAL and renal tubular damage score were significantly increased in group DS and group NIR, the expression of HIF-1α and SLC7A11 was down-regulated in group DS, and the expression of HIF-1α and SLC7A11 was up-regulated in group NIR ( P<0.05). Compared with group DS, the concentrations of serum Cr, BUN and NGAL and renal tubular damage score were significantly increased, and the expression of HIF-1α and SLC7A11 was up-regulated in group DIR ( P<0.05). Compared with group NIR, the concentrations of serum Cr, BUN and NGAL and renal tubular damage score were significantly increased, and the expression of HIF-1α and SLC7A11 was down-regulated in group DIR ( P<0.05). Compared with group DIR, the concentrations of serum Cr, BUN and NGAL and renal tubular damage score were significantly decreased, and the expression of HIF-1α and SLC7A11 was up-regulated in group DIR+ DMOG ( P<0.05). Conclusion:HIF-1α is involved in the renal injury induced by myocardial I/R, which is related to regulation of the expression of SLC7A11 in rats.

5.
Article in Chinese | WPRIM | ID: wpr-911231

ABSTRACT

Objective:To evaluate the relationship between protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway-mediated endoplasmic reticulum stress and the reduction of cerebral ischemia-reperfusion (I/R) injury by dexmedetomidine in mice by the in vivo experiment and the cell experiment. Methods:In the in vivo experiment, 20 healthy clean-grade male mice, aged 6-8 weeks, weighing 20-30 g, were divided into 4 groups ( n=5 each) using a random number table method: sham operation group (group S), sham operation+ dexmedetomidine group (group SD), cerebral I/R group (group IR) and cerebral I/R+ dexmedetomidine group (group IRD). Cerebral I/R was established by two-vessel occlusion plus hypotension.Dexmedetomidine 25 μg/kg was intraperitoneally injected at 10 min of ischemia in group IRD and at the corresponding time point in group SD.Neurological function was assessed using modified neurological severity score at 1 h of reperfusion.The animals were then sacrificed and brain tissues were taken for determination of the expression of endoplasmic reticulum stress-related proteins such as immunoglobulin heavy chain-binding protein (BIP), eukaryotic translation initiation factor 2α (EIF-2α), phosphorylated EIF-2α (p-EIF-2α), PERK and phosphorylated PERK (p-PERK) (by Wester blot). In the cell experiment, a mouse hippocampal neuronal cell line was selected and divided into 4 groups ( n=12 each) using a random number table method: control group (group C), oxygen-glucose deprivation/restoration (OGD/R) group (group OGD/R), OGD/R+ dexmedetomidine group (group OGD/R+ D) and OGD/R+ ISRIB (PERK pathway inhibitor) group (group OGD/R+ ISRIB). Cells were exposed to 94%N 2-5%CO 2-1%O 2 and incubated in a low-glucose DMEM medium for 6 h followed by restoration to establish OGD/R model.At 30 min before OGD, dexmedetomidine (final concentration 5 mmol/L) was added in group OGD/R+ D, and ISRIB (final concentration 10 mmol/L) was added in group OGD/R+ ISRIB.After 12-h restoration was completed, the cell survival rate was detected by CCK-8 assay.At 24 of restoration, the expression of endoplasmic reticulum stress-related proteins was determined by Wester blot. Results:In the in vivo experiment, compared with group S, neurobehavioral score was significantly increased and the expression of BIP, p-EIF-2α and p-PERK in brain tissues was up-regulated in group IR ( P<0.05). Compared with group IR, neurobehavioral score was significantly decreased and the expression of BIP, p-EIF-2α and p-PERK in brain tissues was down-regulated in group IRD ( P<0.05). In the cell experiment, compared with group C, the expression of BIP, p-EIF-2α, PERK and p-PERK was significantly up-regulated, and the cell survival rate was decreased in group OGD/R ( P<0.05). Compared with group OGD/R, the expression of BIP, p-EIF-2α, PERK and p-PERK was significantly down-regulated, and the cell survival rate was increased in OGD/R+ D, OGD/R+ ISRIB groups ( P<0.05). Compared with group OGD/R+ ISRIB, the expression of PERK was significantly down-regulated ( P<0.05) and no significant change was found in the other parameters in group OGD/R+ D ( P>0.05). Conclusion:The mechanism by which dexmedetomidine reduces cerebral I/R injury may be related to inhibiting PERK pathway-mediated endoplasmic reticulum stress in mice.

6.
Article in Chinese | WPRIM | ID: wpr-911214

ABSTRACT

Objective:To evaluate the role of Notch1/hairy and enhancer of split homolog1(Hes1) signaling pathway in high glucose and hypoxia-reoxygenation (H/R) injury to cardiomyocytes.Methods:H9c2 cardiomyocytes were cultured in low-glucose DMEM culture medium supplemented with 10% fetal bovine serum.The cells were divided into 6 groups ( n=12 each) using a random number table method: control group (group C), H/R group, H/R+ Jagged-1 group (group H/R+ J), high glucose group (group HG), high glucose+ H/R group (group HG+ H/R) and high glucose+ H/R+ Jagged-1 group (group HG+ H/R+ J). The cells were incubated in low-glucose culture medium for 72 h in group C. After incubated in low-glucose culture medium for 72 h, the cells were exposed to 24-h hypoxia in an incubator filled with 95% N 2-5% CO 2 at 37℃, immediately followed by 6-h reoxygenation in an incubator filled with 95% O 2-5% CO 2 at 37℃ in group H/R.In group H/R+ J, Jagged-1 (Notch1/Hes1 signaling pathway specific activator) 5μg/ml was added to low-glucose culture medium and the cells were incubated for 72h before H/R.In group HG, H9c2 cardiomyocytes were incubated in high-glucose culture medium containing 33 mmol/L glucose for 72 h. In group HG+ H/R, the cells were incubated in high-glucose medium for 72 h before H/R.In group HG+ H/R+ J, Jagged-1 5μg/ml was added to high-glucose culture medium, and the cells were incubated for 72 h before H/R.At 6 h of reoxygenation, the supernatant of the culture medium was collected for detection of the activities of superoxide dismutase (SOD) and lactic dehydrogenase (LDH), the cell viability (by CCK-8 assay) and the cell apoptosis rate (by flow cytometry) and for determination of expression of Notch1, Hes1 and c-caspase-3 (by Western blot). Results:Compared with group C, the cell survival rate and SOD activity were significantly decreased, and apoptosis rate and LDH activity were increased in H/R, H/R+ J and HG groups, expression of Notch1, Hes1 and c-caspase-3 was up-regulated in H/R and H/R+ J groups, and the expression of Notch1 and Hes1 was down-regulated and c-caspase-3 expression was up-regulated in group HG ( P<0.05). Compared with group H/R, the cell survival rate and SOD activity was significantly increased, apoptosis rate and LDH activity were decreased, expression of Notch1 and Hes1 was up-regulated, and c-caspase-3 expression was down-regulated in group H/R+ J, and the cell survival rate and SOD activity were significantly decreased, apoptosis rate and LDH activity were increased, expression of Notch1 and Hes1 was down-regulated, and c-caspase-3 expression was up-regulated in group HG+ H/R ( P<0.05). Compared with group HG, the cell survival rate and SOD activity were significantly decreased, and apoptosis rate and LDH activity were increased in HG+ H/R and HG+ H/R+ J groups ( P<0.05), and expression of Notch1 and Hes1 was down-regulated, and c-caspase-3 expression was up-regulated in group HG+ H/R ( P<0.05). Compared with group HG+ H/R, the cell survival rate and SOD activity were significantly increased, apoptosis rate and LDH activity were decreased, expression of Notch1 and Hes1 was up-regulated, and c-caspase-3 expression was down-regulated in group HG+ H/R+ J ( P<0.05). Compared with group H/R+ J, the cell survival rate and SOD activity were significantly decreased, apoptosis rate and LDH activity were increased, expression of Notch1 and Hes1 was down-regulated, and c-caspase-3 expression was up-regulated in group HG+ H/R+ J ( P<0.05). Conclusion:Activation of Notch1/Hes1 signaling pathway is the endogenous protective mechanism of high glucose and H/R injury to cardiomyocytes.

7.
Article in Chinese | WPRIM | ID: wpr-911199

ABSTRACT

Objective:To evaluate the role of nuclear factor E2-related factor 2 (NRF2) in myocardial ischemia-reperfusion (I/R) injury and the relationship with ferroptosis in diabetic rats.Methods:Forty-eight SPF healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-220 g, were divided into 5 groups by a random number table method: sham operation group (group S, n=6), myocardial I/R group (group NIR, n=12), diabetes mellitus+ sham operation group (group DS, n=6), diabetes mellitus+ myocardial I/R group (group DIR, n=12) and diabetes mellitus+ myocardial I/R+ NRF2 agonist sulforaphane group (group DIR+ SFN, n=12). Type 1 diabetes mellitus was induced by intraperitoneal injection of 1% streptozotocin-citrate buffer 60 mg/kg.Sulforaphane 500 μg·kg -1·d -1 was injected intraperitoneally before ischemia for 3 consecutive days in group DIR+ SFN.At the 8th week after establishing the model, myocardial I/R was produced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by reperfusion.At 2 h of reperfusion, the left ventricular systolic pressure (LVSP), HR, and the maximum rate of increase and decrease of left ventricular systolic pressure (±dp/dt max) were recorded.Blood samples were taken from the carotid artery and the animals were then sacrificed for determination of concentration of cardiac troponin I (cTnI) in serum (using enzyme-linked immunosorbent assay), myocardial Fe 2+ and malondialdehyde (MDA) contents, superoxide dismutase (SOD) activity (by colorimetry) and myocardial infarct size (using TTC) and for determination of expression of NRF2, ferroportin1 (FPN1) and acyl-CoA synthetase long-chain family member 4 (ACSL4) (by Western blot), and the pathological changes of lung tissues were observed by hematoxylin-eosin staining. Results:Compared with group S, LVSP, HR, and ±dp/dt max were significantly decreased, serum cTnI concentration and myocardial Fe 2+ and MDA contents were increased, SOD activity was decreased, expression of ACSL4 was up-regulated and expression of NRF2 and FPN1 was down-regulated in group NIR ( P<0.05). Compared with group DS, LVSP, HR, and ±dp/dt max were significantly decreased, serum cTnI concentration and myocardial Fe 2+ and MDA contents were increased, SOD activity was decreased, expression of ACSL4 was up-regulated and expression of NRF2 and FPN1 was down-regulated in group DIR ( P<0.05). Compared with group NIR, LVSP, HR, and ±dp/dt max were significantly decreased, serum cTnI concentration and myocardial Fe 2+ and MDA contents were increased, SOD activity was decreased, myocardial infarct size was increased, expression of ACSL4 was up-regulated and expression of NRF2 and FPN1 was down-regulated in group DIR ( P<0.05). Compared with group DIR, LVSP, HR, and ±dp/dt max were significantly increased, serum cTnI concentration and myocardial Fe 2+ and MDA contents were decreased, SOD activity was increased, myocardial infarct size was decreased, expression of ACSL4 was down-regulated and expression of NRF2 and FPN1 was up-regulated in group DIR+ SFN ( P<0.05). Conclusion:NRF2 is involved in the process of myocardial I/R injury, which is related to promoting ferroptosis in diabetic rats

8.
Article in Chinese | WPRIM | ID: wpr-911195

ABSTRACT

Objective:To evaluate the effects of esketamine on pyrolysis in lung tissues of rats with endotoxin-induced acute lung injury (ALI).Methods:SPF healthy adult male Sprague-Dawley rats, weighing 200-220 g, aged 8 weeks, were divided into 3 groups ( n=10 each) using a random number table method: control group (group C), endotoxin-induced ALI group (group ALI) and esketamine group (group E). Lipopolysaccharide (LPS) 10 mg/kg was intraperitoneally injected to establish the model of endotoxin-induced ALI model.The equal volume of 0.9% sodium chloride injection was intraperitoneally injected in group C. Esketamine 10 mg/kg was intraperitoneally injected at 30 min of injection of LPS in group E. Lung tissues were removed after blood samples were collected from hearts at 24 h after injection of LPS for determination of concentrations of serum interleukin-1beta (IL-1β) and IL-8 (by enzyme-linked immunosorbent assay), the wet/dry weight ratio (W/D ratio), activities of myeloperoxidase (MPO) (by colorimetric assay) and the expression of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), caspase-1 and gasdermin D (GSDMD) (by Western blot) and for examination of pathological changes which were scored after haematoxylin and eosin staining and ultrastructure (using an electron microscope). Results:Compared with group C, the lung injury score, W/D ratio, MPO activity, expression of NLRP3, caspase-1 and GSDMD and concentrations of IL-1β and IL-18 in serum were significantly increased in ALI and E groups ( P<0.05). Compared with group ALI, the lung injury score, W/D ratio, MPO activity, expression of NLRP3, caspase-1 and GSDMD and concentrations of IL-1β and IL-18 in serum were significantly decreased in group E ( P<0.05). Conclusion:The mechanism by which esketamine reduces endotoxin-induced ALI is related with inhibition of pyrolysis in lung tissues of rats.

9.
Article in Chinese | WPRIM | ID: wpr-911186

ABSTRACT

Objective:To evaluate the relationship between silence information regulator 1 (SIRT1) and signal transducers and activators of transcription 3 (STAT3) acetylation during high glucose-induced cardiac microvascular endothelial cell injury.Methods:Cardiac microvascular endothelial cells of Sprague-Dawley rats were cultured.The cells at the logarithmic growth phase were selected and divided into 3 groups ( n=24 each) using a random number table method: control group (C group), high glucose group (HG group) and high glucose+ SIRT1 agonist SRT1720 group (HG+ SRT group). The cardiac microvascular endothelial cells were seeded in a 6- or 96-well cell culture plate at a density of 2×10 5 cells/ml.When the cell density reached 50%, the culture medium was then replaced with high-glucose (glucose 33 mmol/L) DMEM culture medium containing with 10% fetal bovine serum and 1% double antibody in HG and HG+ SRT groups.In group HG+ SRT, 20 μmol/L SRT1720 was added simultaneously, and the cells were cultured at 37 ℃ in an incubator with 5% CO 2 for 24 h. The cell viability was determined by CCK-8 assay, the activity of superoxide dismutase (SOD) was detected using a spectrophotometer, the levels of lactic dehydrogenase (LDH), interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) in the supernatant were detected by enzyme-linked immunosorbent assay, and the expression of SIRT1, acetylated STAT3 (ac-STAT3) and phosphorylated STAT3 (p-STAT3) was determined by Western blot. Results:Compared with C group, the cell viability and SOD activity were significantly decreased, levels of LDH, IL-6 and TNF-β in the supernatant were increased, expression of SIRT1 was down-regulated, and expression of ac-STAT3 and p-STAT3 was up-regulated in group HG and group HG+ SRT ( P<0.05). Compared with group HG, the cell viability and SOD activity were significantly increased, levels of LDH, IL-6 and TNF-β in the supernatant were decreased, expression of SIRT1 was up-regulated, and expression of ac-STAT3 and p-STAT3 was down-regulated in group HG+ SRT ( P<0.05). Conclusion:SIRT1 can alleviate high glucose-induced cardiac microvascular endothelial cell injury by promoting STAT3 deacetylation.

10.
Article in Chinese | WPRIM | ID: wpr-885077

ABSTRACT

Objective:To evaluate the efficacy of remimazolam-propofol-sufentanil for anesthesia in patients undergoing painless gastroscopy.Methods:Eighty American Society of Anesthesiologists physical statusⅠor Ⅱ patients, aged 20-59 yr, weighing 44-69 kg, scheduled for elective painless gastroscopy, were divided into 2 groups ( n=40 each) using a random number table method: remimazolam-propofol-sufentanil group (group RPS) and propofol-sufentanil group (group PS). The patients in group RPS received successive intravenous injection of sufentanil 0.1 μg/kg, remimazolam 0.15 mg/kg and propofol (at a rate of 4 mg/s). The patients in group PS received intravenous injection of sufentanil 0.1 μg/kg and propofol (at a rate of 4 mg/s). When Observer′ s Assessment of Alertness/Sedation Scale score was 0, gastroscopy was performed.The consumption of propofol, time of anesthesia, time for gastroscopy, emergence time and discharge time were recorded.The number of intraoperative assisted respiration cases, body movement and occurrence of adverse reactions at the time of discharge were observed. Results:Compared with group PS, the consumption of propofol was significantly decreased, and the time of anesthesia, emergence time and discharge time were shortened in group RPS ( P<0.05). There was no significant difference in the time for gastroscopy, the number of intraoperative assisted respiration cases, body movement and the occurrence of adverse reactions at discharge time between the 2 groups ( P>0.05). Conclusion:Remimazolam-propofol-sufentanil produces better efficacy for anesthesia than propofol-sufentanil in patients undergoing painless gastroscopy.

11.
Article in Chinese | WPRIM | ID: wpr-885073

ABSTRACT

Objective:To evaluate the effects of esketamine on myocardial injury and the relationship with nuclear factor-erythroid 2-related factor 2 (Nrf2) heme oxygenase-1 (HO-1) signaling pathway in septic rats.Methods:Thirty-two SPF healthy adult male Sprague-Dawley rats, weighing 200-230 g, were randomized into 4 groups ( n=8 each) using a random number table method: control group (group C), control plus esketamine group (group CE), sepsis group (group S) and sepsis plus esketamine group (group SE). Lipopolysaccharide (LPS) 10 mg/kg was intraperitoneally injected to establish the sepsis model.At 30 min after LPS or normal saline intraperitoneal injection, esketamine 10 mg/kg was intraperitoneally injected, and administration was repeated 12 h later in group SE and group CE.At 24 h after LPS injection, left ventricular ejection fraction (LVEF) was measured (using echocardiography), and serum cardiac troponin I (cTnI), brain natriuretic peptide (BNP), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), tumor necrosis factor alpha (TNF-α) and high mobility group box-1 (HMGB1) concentrations were determined (by enzyme linked immunosorbent assay). Myocardial tissues were obtained for examination of pathological changes (by hematoxylin-eosin staining) and for determination of expression of Nrf2, HO-1 and transcription factor Bach 1 (BTB-CNC allogeneic 1). Results:Compared with group C, LVEF was significantly decreased, concentrations of cTnI, BNP, LDH, CK-MB, TNF-α and HMGB1 in serum were increased, expression of Nrf2 and HO-1 was down-regulated, and expression of Bach 1 was up-regulated ( P<0.05), and the significant pathological changes of myocardial tissues were found in S and SE groups.No significant change was found in the parameters mentioned above in group CE ( P>0.05). Compared with group S, LVEF was significantly increased, concentrations of cTnI, BNP, LDH, CK-MB, TNF-α and HMGB1 in serum were decreased, expression of Nrf2 and HO-1 was up-regulated, and expression of Bach 1 was down-regulated ( P<0.05), and the pathological changes of myocardium were significantly attenuated in group SE. Conclusion:Esketamine can reduce myocardial injury, and the mechanism may be related to activating Nrf2/HO-1 signaling pathway in septic rats.

12.
Article in Chinese | WPRIM | ID: wpr-885060

ABSTRACT

Objective:To evaluate the role of autophagy in reduction of high glucose and hypoxia-reoxygenation (HG+ H/R) injury to isolated cardiomyocytes by dexmedetomidine in rats.Methods:The normally cultured rat H9c2 cardiomyocytes at the logarithmic growth phase were seeded in 6-well plates at a density of 1×10 6 cells/ml and divided into 4 groups ( n=15 each) using a random number table method: control group (group C), group HG+ H/R, dexmedetomidine group (group DEX) and dexmedetomidine+ autophagy inhibitor 3-methylpurine group (group 3-MA). The cells were incubated in culture medium with 1% fetal bovine serum + 1% double antibody for 24 h when the cell density reached 50%.To establish HG+ H/R injury model, the cardiomyocytes were cultured in high-glucose culture medium (glucose concentration of 33 mmol/L) for 24 h, and then incubated in a 37 ℃ incubator (95% N 2+ 5%CO 2) for 4 h followed by reoxygenation (90%O 2+ 10%CO 2) for 2 h. Dexmedetomidine was added until the final concentration reached 5 μmol/L at 1 h before hypoxia in DEX and 3-MA groups, and 3-MA was added until the final concentration reached 5 μmol/L at 1 h of incubation with dexmedetomidine.At 2 h after reoxygenation, the cell viability was recorded by the cell counting kit-8 assay, lactate dehydrogenase (LDH) activity was detected by LDH kit, the expression of autophagy-related protein LC3, P62 and Beclin-1 was detected by Western Blot, the ratio of LC3Ⅱ/LC3Ⅰwas calculated, and the expression of P62 and Beclin-1 mRNA was detected by real-time polymerase chain reaction. Results:Compared with group C, the cell viability was significantly decreased in HG+ H/R, DEX and 3-MA groups, LDH activity in the supernatant was increased and expression of P62 was decreased in HG+ H/R and 3-MA groups, ratio of LC3Ⅱ/LC3Ⅰwas decreased in group 3-MA, and the expression of Beclin-1 was down-regulated in group HG+ H/R ( P<0.05). Compared with HG+ H/R group, LDH activity in the supernatant was significantly decreased, expression of Beclin-1, P62 and its mRNA was up-regulated, and ratio of LC3Ⅱ/LC3Ⅰwas increased in DEX group, and LDH activity in the supernatant was increased in group 3-MA ( P<0.05). Compared with DEX group, cell viability were decreased, LDH activity in the supernatant was increased, Beclin-1, P62 and its mRNA was down-regulated, and ratio of LC3Ⅱ/ LC3Ⅰwas decreased in group 3-MA ( P<0.05). Conclusion:Autophagy is involved in the reduction of HG+ H/R injury to isolated cardiomyocytes by dexmedetomidine in rats.

13.
Article in Chinese | WPRIM | ID: wpr-885055

ABSTRACT

Objective:To evaluate the role of nuclear receptor subfamily 1, group D, member 1/brain and muscle Arnt-like 1(Rev-erbα/Bmal1) signaling pathway in myocardial ischemia-reperfusion (I/R) injury in diabetic rats and its relationship with autophagy.Methods:SPF-grade adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-220 g, were used in this study.Type I diabetes mellitus was induced by intraperitoneal streptozotocin 60 mg/kg.The rats were continuously fed for 8 weeks after successful establishment of the model.Thirty rats with type 1 diabetes mellitus were divided into 3 groups by a random number table method: diabetic sham operation group (DS group, n=6), diabetic myocardial I/R group (DI/R group, n=12) and diabetic myocardial I/R plus Rev-erbα antagonist SR-8278 group (DI/R+ SR group, n=12). Eighteen non-diabetic rats were divided into 2 groups by a random number table method: non-diabetic sham operation group (NS group, n=6) and non-diabetic myocardial I/R group (NI/R group, n=12). The myocardial I/R model was established by ligation of the left anterior descending coronary artery for 30 min followed by 120-min reperfusion in anesthetized rats.SR-8278 2 mg/kg was intravenously injected via the femoral vein at 1 h before ischemia in group DI/R+ SR.Blood samples were collected from the carotid artery immediately after the end of reperfusion for determination of serum troponin I (cTnI), creatine kinase-MB (CK-MB) and lactic dehydrogenase (LDH) levels (by enzyme-linked immunosorbent assay). Then the rats were sacrificed, and myocardial tissues were obtained for determination of myocardial infarct size (by TTC method), expression of Rev-erbα and Bmal1 mRNA (by real-time polymerase chain reaction) and expression of Rev-erbα, Bmal1, microtubule-associated protein 1 light chain (LC3) Ⅱ and LC3Ⅰ (by Western blot) and for calculation of the ratio of LC3 Ⅱ/LC3Ⅰand the number of autophagosomes (with a transmission electron microscope). Results:Compared with group NS, the percentage of myocardial infarct size, serum levels of cTnI, CK-MB and LDH and the number of autophagosomes were significantly increased, the expression of Rev-erbα and its mRNA in myocardial tissues was up-regulated, the expression of Bmall and its mRNA was down-regulated, and the ratio of LC3 Ⅱ/LC3Ⅰwas increased in group NI/R, and serum levels of cTnI, CK-MB and LDH were increased, the number of autophagosomes was decreased, the expression of Rev-erbα and its mRNA in myocardial tissues was up-regulated, the expression of Bmall and its mRNA was down-regulated and the ratio of LC3 Ⅱ/LC3Ⅰwas decreased in group DS ( P<0.05). Compared with group NI/R, the percentage of myocardial infarct size and serum levels of cTnI, CK-MB and LDH were significantly increased, the number of autophagosomes was decreased, the expression of Rev-erbα and its mRNA in myocardial tissues was up-regulated, the expression of Bmall and its mRNA was down-regulated, and the ratio of LC3 Ⅱ/LC3Ⅰwas decreased in group DI/R ( P<0.05). Compared with group DS, the percentage of myocardial infarct size, serum levels of cTnI, CK-MB and LDH and the number of autophagosomes were were significantly increased, the expression of Rev-erbα and its mRNA in myocardial tissues was up-regulated, the expression of Bmall and its mRNA was down-regulated, and the ratio of LC3 Ⅱ/LC3Ⅰwas increased in group DI/R ( P<0.05). Compared with group DI/R, the percentage of myocardial infarct size, serum levels of cTnI, CK-MB and LDH and the number of autophagosomes were significantly decreased, the expression of Rev-erbα and its mRNA in myocardial tissues was down-regulated, the expression of Bmall and its mRNA was up-regulated, and the ratio of LC3 Ⅱ/LC3Ⅰwas increased in group DI/R+ SR ( P<0.05). Conclusion:Rev-erbα/BMAL1 signaling pathway is involved in the process of myocardial I/R injury by regulating cell autophagy in diabetic rats.

14.
Article in Chinese | WPRIM | ID: wpr-869969

ABSTRACT

Objective:To evaluate the role of hippocampal histone deacetylases (HDACs) in perioperative neurocognitive disorders (PND) and the relationship with postsynaptic dense protein 95 (PSD95) in rats.Methods:Sixty clean-grade healthy male Sprague-Dawley rats, aged 10-14 weeks, weighing 250-280 g, were divided into 3 groups ( n=20 each) using a random number table method: control group (group C), surgery group (group S) and HDAC inhibitor MS-275 group (group MS-275). Exploratory laparotomy was performed under 3% sevoflurane anesthesia in group S. MS-275 10 mg/kg was intraperitoneally injected at 0.5 h before exploratory laparotomy in group MS-275.Morris water maze tests were performed on 1 day before surgery and 1, 3 and 7 days after surgery.Ten rats were sacrificed on 1 day after surgery, and hippocampal tissues were obtained for determination of the expression of HDAC1-3 and PSD95 protein and mRNA by Western blot and real-time polymerase chain reaction, respectively.The density of hippocampal neurons was determined by the Nissl staining. Results:Compared with group C, the postoperative escape latency was significantly prolonged, the number of crossing the original platform was decreased, the density of hippocampal neurons was decreased, the expression of HDAC2 protein and mRNA was up-regulated, and the expression of PSD95 protein and mRNA was down-regulated in group S ( P<0.05 or 0.01). Compared with group S, the postoperative escape latency was significantly shortened, the number of crossing the original platform was increased, the density of hippocampal neurons was increased, the expression of HDAC2 protein and mRNA was down-regulated, and the expression of PSD95 protein and mRNA was up-regulated in group MS-275 ( P<0.05 or 0.01). There was no significant difference in the expression of HDAC1 and HDAC3 protein and mRNA among the three groups ( P>0.05). Conclusion:HDAC2 is involved in the pathophysiological mechanism of PND by down-regulating the expression of PSD95 in rats.

15.
Article in Chinese | WPRIM | ID: wpr-869930

ABSTRACT

Objective:To evaluate the role of long-chain non-coding RNA-lung cancer metastasis-related transcript 1/microRNA-145/Bcl-2 and adenovirus E1B19k Da interacting protein 3 (Lnc-MALAT1/miRNA-145/BNIP3) signaling pathway in sufentanil preconditioning-induced cardioprotection in rats.Methods:Rat H9C2 cells were inoculated in 6-well culture plates or flasks at a density of 1×10 6 cells/ml and divided into 5 groups ( n=30 each) using a random number table method: control group (group C), hypoxia-reoxygenation (H/R) group, sufentanil preconditioning group (S group), eukaryotic expression vector pcDNA3.0 group (pcDNA group) and pcDNA-MALAT1 group (MALAT1 group). Cells were incubated with 10 μmol/L sufentanil for 2 h, and then the H/R injury model was established in group S. In pcDNA group and MALAT1 group, cells were transfected with pcDNA3.0 and pcDNA-MALAT1, respectively, and then incubated with 10 μmol/L sufentanil for 2 h starting from 24 h after transfection, and then the H/R injury model was established.At 2 h after reoxygenation, the expression of Lnc-MALAT1, miRNA-145 and BNIP3 mRNA was detected by real-time polymerase chain reaction, the cell survival rate was detected by CCK-8, the apoptosis rate was detected by flow cytometry, the malondialdehyde (MDA) and superoxide dismutase (SOD) levels and amount of lactic dehydrogenase (LDH) released were detected, and the expression of Bcl-2, Bax and cleaved-caspase-3 was detected by Western blot. Results:Compared with group C, the survival rate was significantly decreased, apoptosis rate was increased, the MDA level and amount of LDH released were increased, SOD levels were decreased, the expression of LncRNA-MALAT1, BNIP3 mRNA, Bax, and cleaved-caspase-3 was up-regulated, and miRNA-145 and Bcl-2 expression was down-regulated in the other four groups ( P<0.05). Compared with group H/R, the cell survival rate was significantly increased, apoptosis rate was decreased, the MDA level and amount of LDH released were decreased, SOD levels were increased, the expression of LncRNA-MALAT1, BNIP3 mRNA, Bax, and cleaved-caspase-3 was down-regulated, and miRNA-145 and Bcl-2 expression was up-regulated in S and pcDNA groups ( P<0.05). Compared with group S, the survival rate was significantly decreased, apoptosis rate was increased, MDA level and amount of LDH released were increased, SOD levels were decreased, the expression of LncRNA-MALAT1, BNIP3 mRNA, Bax, and cleaved-caspase-3 was up-regulated, and miRNA-145 and Bcl-2 expression was down-regulated in group MALAT1 ( P<0.05). Conclusion:The mechanism of sufentanil preconditioning-induced cardioprotection is related to inhibiting Lnc-MALAT1/miRNA-145/BNIP3 signaling pathway in rats.

16.
Article in Chinese | WPRIM | ID: wpr-869888

ABSTRACT

Objective:To evaluate the role of c-Abl in myocardial ischemia-reperfusion (I/R) injury in diabetic rats.Methods:Sixty male SPF-grade healthy Sprague-Dawley rats, aged 7-9 weeks, weighing 210-230 g, were divided into 6 groups by a random number table method: sham operation group (S group, n=6), myocardial I/R group (IR group, n=12), diabetic sham operation group (DS group, n=6), diabetic myocardial I/R group (DIR group, n=12), diabetic myocardial I/R plus AVV9-siRNA-c-Abl group (DIR+ c-Abl group, n=12), and diabetic myocardial I/R plus AVV9-GFP group (DIR+ GFP group, n=12). One percent streptozotocin 60 mg/kg was intraperitoneally injected to induce type 1 diabetes mellitus.AVV9-siRNA-c-Abl and AVV9-GFP 1×10 12 mg/kg were slowly injected at 4 weeks after establishing the model in DIR+ c-Abl and DIR+ GFP groups.Myocardial ischemia was induced by 30 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 2 h reperfusion at 8 weeks after establishing the model.At the end of reperfusion, left ventricular systolic pressure (LVSP) and the maximum rate of increase and decrease of left ventricular systolic pressure (±dp/dt max) were monitored, and blood samples were collected for determination of the concentrations of serum lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB) (by enzyme-linked immunosorbent assay)and myocardial infarct size (except group S and group DS). Myocardial tissues were obtained for determination of the apoptosis index of cardiomyocytes(by TUNEL staining), expression of c-Abl, p53 and activated caspase-3 (by Western blot), and binding of c-Abl and p53 (c-Abl/p53) (by co-immunoprecipitation method). Results:LVSP and ±dp/dt max were significantly decreased, serum LDH and CK-MB concentrations were increased, apoptosis index and c-Abl/p53 were increased, and the expression of c-Abl, p53 and activated caspase-3 was up-regulated in group IR when compared with group S and in group DIR as compared with group DS ( P<0.05). Compared with group DIR, the LVSP and ± dp/dt max were significantly increased, serum LDH and CK-MB concentrations were decreased, myocardial infarct size was decreased, apoptosis index and c-Abl/p53 were decreased, and the expression of c-Abl, p53 and activated caspase-3 was down-regulated in group DIR+ c-Abl ( P<0.05), and no significant change was found in the parameters mentioned above in group DIR+ GFP ( P>0.05). Conclusion:c-Abl is involved in the pathophysiological process of myocardial I/R injury probably by activating p53 signaling pathway in diabetic rats.

17.
Article in Chinese | WPRIM | ID: wpr-869882

ABSTRACT

Objective:To evaluate the relationship between silence information regulator 1 (SIRT1) and NOD-like receptor protein 3 (NLRP3) inflammasomes during myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods:SPF-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-220 g, were used in this study.Type 1 diabetes mellitus was induced by intraperitoneal 1% streptozotocin diluted in citrate buffer solution 60 mg/kg.The rats were continuously fed for 8 weeks after successful establishment of the model.Forty-two rats with type 1 diabetes mellitus were divided into 4 groups by a random number table method: diabetic sham operation group (DS group, n=6), diabetic myocardial I/R group (DIR group, n=12), diabetic myocardial I/R plus SIRT1 agonist SRT1720 group (DIR+ SR group, n=12) and diabetic myocardial I/R plus SIRT1 inhibitor EX-527 group (DIR+ EX group, n=12). Eighteen non-diabetic rats were divided into 2 groups by a random number table method: non-diabetic sham operation group (NS group, n=6) and non-diabetic myocardial I/R group (NIR group, n=12). The myocardial I/R model was established by ligation of the left anterior descending coronary artery for 30 min followed by 120-min reperfusion in anesthetized rats.Blood samples were collected from the carotid artery immediately after the end of reperfusion for determination of serum troponin I (cTnI), creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) levels (by enzyme-linked immunosorbent assay). Then the rats were sacrificed, and myocardial tissues were obtained for determination of myocardial infarct size (by TTC method) and expression of SIRT1, NLRP3 and IL-1β (by Western blot) and for microscopic examination of pathological changes of myocardial tissues (by HE staining). The percentage of myocardial infarct size was calculated. Results:Compared with group NS, the serum levels of cTnI, CK-MB and LDH were significantly increased, the expression of SIRT1 in myocardial tissues was down-regulated, and the expression of NLRP3 and IL-1β was up-regulated in group NIR ( P<0.05). Compared with group DS, the serum levels of cTnI, CK-MB and LDH were significantly increased, the expression of SIRT1 in myocardial tissues was down-regulated, and the expression of NLRP3 and IL-1β was up-regulated in group DIR ( P<0.05). Compared with group NIR, the percentage of myocardial infarct size and serum levels of cTnI, CK-MB and LDH were significantly increased, the expression of SIRT1 in myocardial tissues was down-regulated, the expression of NLRP3 and IL-1β was up-regulated ( P<0.05), and the pathological changes were accentuated in group DIR.Compared with group DIR, the percentage of myocardial infarct size and serum levels of cTnI, CK-MB and LDH were significantly decreased, the expression of SIRT1 in myocardial tissues was up-regulated, the expression of NLRP3 and IL-1β was down-regulated ( P<0.05), and the pathological changes were significantly attenuated in group DIR+ SR, and the percentage of myocardial infarct size and serum levels of cTnI, CK-MB and LDH were significantly increased, the expression of SIRT1 in myocardial tissues was down-regulated, the expression of NLRP3 and IL-1β was up-regulated ( P<0.05), and the pathological changes were accentuated in group DIR+ EX. Conclusion:The up-regulated expression of SIRT1 can inhibit the activation of NLRP3 inflammasomes and produces endogenous protection during myocardial I/R in diabetic rats.

18.
Article in Chinese | WPRIM | ID: wpr-869873

ABSTRACT

Objective:To evaluate the role of autophagy in ischemia postconditioning (IPO)-induced attenuation of intestinal ischemia-reperfusion (I/R) injury in mice.Methods:Thirty-two SPF healthy adult male C57BL/6J mice, aged 9-12 weeks, weighing 25-29 g, were divided into 4 groups ( n=8 each) using a random number table method: sham operation group (group S), intestinal I/R group (group IIR), group IPO and IPO plus 3-methyladenine (3-MA) group (group IPO+ 3-MA). The model of intestinal I/R was established by occlusion of superior mesenteric artery for 45 min followed by 2-h reperfusion in anesthetized animals.The mice underwent 3 cycles of 30-s reperfusion followed by 30-s ischemia before restoration of reperfusion in group IPO.Blood samples from the femoral artery were collected at 2 h of reperfusion for determination of concentrations of serum diamine oxidase (DAO), D-lactate (D-LA) and intestinal fatty acid binding protein (I-FABP). The animals were then sacrificed and intestinal tissues were removed for microscopic examination of the pathologic changes which were scored according to Chiu and for determination of the expression of autophagy-related proteins Beclin-1 and p62 (by Western blot). The water content of intestinal tissues was calculated. Results:Compared with group S, the Chiu′s score, concentrations of serum DAO, D-LA and I-FABP, water content of intestinal tissues, and LC3Ⅱ/LC3Ⅰ ratio were significantly increased, Beclin-1 expression was up-regulated, and p62 expression was down-regulated in IIR, IPO and IPO+ 3-MA groups ( P<0.05). Compared with group IIR, the Chiu′s score, concentrations of serum DAO, D-LA and I-FABP, water content of intestinal tissues, and LC3Ⅱ/LC3Ⅰ ratio were significantly decreased, Beclin-1 expression was up-regulated, and p62 expression was down-regulated in group IPO ( P<0.05). Compared with group IPO, the Chiu′s score, concentrations of serum DAO, D-LA and I-FABP, and water content of intestinal tissues were significantly increased, LC3Ⅱ/LC3Ⅰratio was decreased, Beclin-1 expression was down-regulated, and p62 expression was up-regulated in group IPO+ 3-MA ( P<0.05). Conclusion:Autophagy is involved in ischemia postconditioning-induced attenuation of intestinal I/R injury in mice.

19.
Article in Chinese | WPRIM | ID: wpr-869851

ABSTRACT

During the epidemic of coronavirus disease 2019 (COVID-19), the infection of the elderly population will bring great challenges to clinical diagnosis and treatment, outcome and management.Combined with the characteristics of anesthesia and the pathophysiological characteristics of COVID-19 on lung function impairment in elderly patients, Chinese Society of Anesthesiology formulated the " Recommendations for anesthesia management and infection control in elderly patients with COVID-19″. This recommendation expounds preoperative visit and infection control, anesthesia management protocol, anesthesia monitoring, anesthesia induction/endotracheal intubation, anesthesia maintenance and infection control, intraoperative lung protection strategy, anti-stress and anti-inflammatory management, hemodynamic optimization, infection control during emergence from anesthesia, and postoperative analgesia in elderly patients with COVID-19, and provides the reference for the safe and effective implementation of anesthesia management in elderly patients during the prevention and control of COVID-19 epidemic.

20.
Acta cir. bras ; 35(1): e202000106, 2020. graf
Article in English | LILACS | ID: biblio-1088526

ABSTRACT

Abstract Purpose To explore the role of all-trans retinoic acid (ATRA) in renal ischemia/reperfusion injury of diabetic rats. Methods Sixty adult male rats were randomly divided into 6 groups, including sham group (S group), ischemia-reperfusion group (I/R group), ischemia-reperfusion+ATRA group (A group), diabetic group (D group), diabetic ischemia-reperfusion group (DI/R group), diabetic ischemia-reperfusion +ATRA group (DA group). The levels of creatinine (Cr), cystatin C (Cys-C) and β2-microglobulin (β2-MG) were measured. Morphology of renal tissue was observed under light microscope. Results DJ-1, Nrf2, HO-1 and caspase-3 were detected by western blot. DJ-1, Nrf2, HO-1 and caspase-3 in I/R group, D group and DI/R group was higher than that in S group. Compared with I/R group, Nrf2 and HO-1 in A group was decreased, but caspase-3 was increased. However, Nrf2 in DA group was higher than that in DI/R group, HO-1 and caspase-3 in DA group were lower than that in DI/R group. Compared with group S, Cr, Cys-C and β2-MG in I/R group, A group, D group, and DI/R group were higher. Whereas the levels of Cr, Cys-C, β2-MG and renal injury score in DA group were lower than those in DI/R group. Conclusion ATRA has a protective effect on renal ischemia-reperfusion injury in diabetic rats, maybe relating to DJ/Nrf2 pathway.


Subject(s)
Animals , Male , Rats , Tretinoin/therapeutic use , Reperfusion Injury/prevention & control , Diabetes Mellitus, Experimental/chemically induced , NF-E2-Related Factor 2/therapeutic use , Kidney/drug effects , Tretinoin/pharmacology , Reperfusion Injury/pathology , Streptozocin , Disease Models, Animal , Drug Evaluation, Preclinical , NF-E2-Related Factor 2/pharmacology , Kidney/pathology
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