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1.
Article in English | WPRIM | ID: wpr-922119

ABSTRACT

OBJECTIVE@#To assess the clinical effectiveness of acupoint application (AP) of Guan Xin Su He Pill (, GXSHP) for patients with chronic stable angina pectoris (CSAP).@*METHODS@#This study was carried out in 3 local hospitals in Chengdu, China. After baseline evaluation, eligible patients were randomly assigned to the placebo application for acupoints (PAA) group or the herbal application for acupoints (HAA) group. Patients in the HAA group underwent AP with herbal powder, which was mainly GXSHP, and patients in the PAA group underwent AP with sham drugs. For each treatment session, unilateral acupoints including Neiguan (PC 6), Danzhong (RN 17), Xinshu (BL 15) and Jueyinshu (BL 14), were stimulated for both groups. AP was performed 3 times a week with a 2-day interval for 4 weeks. The primary outcome was the frequency of angina pectoris attacks per week, while the secondary outcomes included angina pain intensity measured by the Visual Analogue Scale (VAS), dose of rescue oral drugs (nitroglycerin), scores on the Seattle Angina Questionnaire (SAQ), Self-Rating Anxiety Scale scores (SAS) and Self-Rating Depression Scale scores (SDS). Clinical outcomes were measured at week 0, 4 and 8. The safety of AP of GXSHP treatment for CSAP were assessed.@*RESULTS@#A total of 121 patients were enrolled. Baseline characteristics were comparable across the 2 groups. After treatment, the angina attack numbers in the HAA group were significantly reduced from 11.00 to 4.81 (P<0.05). While, for PAA group, the angina frequency was not significantly improved (baseline 10.55; post-treatment 11.05). The HAA group had significantly fewer angina attacks than the PAA group (P<0.05). Pain intensity measured by VAS in HAA group was significantly reduced from 4.06 to 3.02 (P<0.05). While, for PAA group, the VAS was significantly increased (baseline 3.62; post-treatment 3.96; P<0.05). Clinical outcomes showed better improvement after treatment in the HAA group than in the PAA group in terms of oral administration of rescue drugs, SAS, SDS and SAQ scores (P<0.05). The adverse events were also reported.@*CONCLUSION@#AP of GXSHP is a safe and effective treatment for CSAP patients (Registration No. NCT02029118).


Subject(s)
Acupuncture Points , Angina, Stable/drug therapy , China , Drugs, Chinese Herbal/adverse effects , Female , Humans , Male , Treatment Outcome
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-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.

4.
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.

5.
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.

6.
Article in Chinese | WPRIM | ID: wpr-755618

ABSTRACT

Objective To evaluate the role of autophagy in Parkin over-expression-induced reduction of cardiac hypertrophy in diabetic rats.Methods Thirty-two healthy SPF male Sprague-Dawley rats,aged 2 months,weighing 200-230 g,were divided into 4 groups (n =8 each) using a random number table method:non-diabetes mellitus (DM) group (group Non-DM),DM group,DM plus AAV9-CMV-Parkin group (group DM+P) and DM puls AAV9-CMV-Parkin puls autophagy inhibitor 3-methyladenine (3-MA) group (group DM+P+MA).DM was induced by intraperitoneal streptozotocin (STZ) 60 mg/kg and confirmed by blood glucose level >16.7 mmol/L,and Parkin overexpression was achieved with adeno-associated virus serotype 9 as a vector.AAV9-CMV-Parkin 1 × 1012 mg/kg was injected into the tail vein at 3 weeks after STZ injection in group DM+P.In group DM+P+MA,AAV9-CMV-Parkin 1× 1012 mg/kg was injected into the tail vein at 3 weeks after STZ injection,and 3 weeks later 3-MA 15 mg/kg was injected into the tail vein,once a week for 6 weeks in total.Cardiac diastolic and systolic function was detected using Bmode ultrasonography.Cardiomyocytes were obtained for microscopic examination of the cross-sectional area (with a light microscope) and for determination of the expression of microtubule-associated protein 1 light chain 3,P62 and Parkin.Results Compared with group Non-DM,the cross-sectional area of cardiomyocytes was significantly increased,and the diastolic and systolic function was decreased in DM group (P<0.05).Compared with group DM,the cross-sectional area of cardiomyocytes was significantly decreased,the diastolic and systolic function was improved,the expression of microtubule-associated protein 1 light chain 3 and Parkin in myocardial tissues was up-regulated,and the expression of P62 was down-regulated in group DM+P (P<0.05).Compared with group MD+P,the cross-sectional area of cardiomyocytes was significantly increased,the diastolic and systolic function was decreased,the expression of microtubule-associated protein 1 light chain 3 was down-regulated,and the expression of P62 was up-regulated in group DM+P+MA (P<0.05) Conclusion Autophagy is involved in Parkin over-expression-induced reduction of cardiac hypertrophy in diabetic rats.

7.
Chinese Journal of Anesthesiology ; (12): 1237-1239, 2019.
Article in Chinese | WPRIM | ID: wpr-797066

ABSTRACT

Objective@#To evaluate the effect of penehyelidine hydrochloride (PHCD) on tumor necrosis factor α-induced protein 8-like-2 (TIPE2)-Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88) signaling pathway in a rat model of traumatic acute lung injury (ALI).@*Methods@#Thirty SPF healthy male Sprague-Dawley rats, aged 8 weeks, weighing 190-210 g, were divided into 3 groups (n=15 each) by a random number table method: sham operation group (group Sham), traumatic ALI group (group ALI) and group PHCD.ALI was induced by blunt chest trauma in ALI and PHCD groups.PHCD 2 mg/kg was intraperitoneally injected immediately after blunt chest trauma in group PHCD.The rats were sacrificed and lung tissues were removed at 8 h after the model was successfully established for examination of the pathological changes and ultrastructure of lung tissues (with a light microscope or an electron microscope) and for determination of the wet to dry weight ratio (W/D ratio) and expression of TLR4 and MyD88 in lung tissues.@*Results@#Compared with group Sham, the W/D ratio was significantly increased, TIPE2 expression was down-regulated, and the expression of TLR4 and MyD88 was up-regulated in ALI and PHCD groups (P<0.05). Compared with group ALI, the W/D ratio was significantly decreased, TIPE2 expression was up-regulated, and the expression of TLR4 and MyD88 was down-regulated (P<0.05), and the pathological changes of lung tissues and ultrastructure were significantly attenuated in group PHCD.@*Conclusion@#The mechanism by which PHCD reduces traumatic AIL is related to activating TIPE2-TLR4-MyD88 signaling pathway in rats.

8.
Chinese Journal of Anesthesiology ; (12): 1001-1004, 2019.
Article in Chinese | WPRIM | ID: wpr-805828

ABSTRACT

Objective@#To evaluate the relationship between tumor necrosis factor-alpha-induced protein 8-like 2 (TIPE2) and caspase-11 during pyroptosis in macrophages of mice.@*Methods@#J774A.1 macrophages of mice were divided into 4 groups (n=6 each) using a random number table method: non-specific siRNA (Scr-siRNA) group (S group), Scr-siRNA plus LPS/ATP group (S+ LPS/ATP group), TIPE2-siRNA group (T group) and TIPE2-siRNA plus LPS/ATP group (T+ LPS/ATP group). The corresponding siRNA and Lipofectamine2000 transfection reagents were added to each group, and transfection was performed for 24-48 h, and in addition LPS 1.0 μg/ml was then added, cells were incubated for 5 h, then ATP 5.0 mmol/L was added, and cells were incubated for 1 h in S+ LPS/ATP and T+ LPS/ATP groups.Cells were collected to detect the expression of TIPE2, caspase-11, NOD-like receptor familypyrin domain containing 3 (NLRP3) and caspase-1 (by Western blot). The supernatant was collected for determination of lactic dehydrogenase (LDH) and myeloperoxidase (MPO) activities and concentrations of interleukin-1beta (IL-1β) and IL-18 (by enzyme-linked immunosorbent assay).@*Results@#Compared with group S, the expression of TIPE2 was significantly down-regulated, the expression of caspase-11, NLRP3 and caspase-1 was up-regulated, and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group S+ LPS/ATP (P<0.05). Compared with group T, the expression of TIPE2 was significantly down-regulated, the expression of caspase-11, NLRP3 and caspase-1 was up-regulated, and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group T+ LPS/ATP (P<0.05). Compared with group S+ LPS/ATP, the expression of TIPE2 was significantly down-regulated, the expression of caspase-11, NLRP3 and caspase-1 was up-regulated, and and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group T+ LPS/ATP (P<0.05).@*Conclusion@#TIPE2 inhibits pyroptosis in macrophages through down-regulating the expression of caspase-11 in mice.

9.
Chinese Journal of Epidemiology ; (12): 971-975, 2019.
Article in Chinese | WPRIM | ID: wpr-805750

ABSTRACT

Objective@#To investigate the associations between smoking and literacy on health among 4-6 grade primary school students.@*Methods@#A questionnaire survey was conducted to research on health literacy and smoking among 4-6 grade pupils in Shandong province, through a multi-stage stratified cluster random sampling method. Sociodemographic characteristics, health literacy level and smoking rate were collected from respondents. Binary logistic regression analysis was used to evaluate the association of smoking and health literacy.@*Results@#A total of 9 240 questionnaires were distributed, with the rate of valid response as 99.7%. The current smoking rate of the students was 2.6%, on higher in boys (3.1%) than in girls (2.0%). 60.8% of 4-6 grade students were found to have adequate health literacy level. Levels of literacy health in both boy and girl school students appeared 56.7% and 64.9%, respectively. Results indicated that health literacy in smokers (14.4%) was lower than that in non-smokers (62.0%). Results from the binary logistic regression analysis showed that the independent influencing factors would include grade, father’s education level, economic situation of the family, self-assessment on the school record and literacy on health (P<0.01). After controlling the other independent variables, the smoking rate was 8.62 (1/0.116) times in students with low literacy level on health, than those with high literacy level.@*Conclusions@#Literacy on health was significantly associated with smoking in the 4-6 grade pupils of Shandong province.

10.
Chinese Journal of Anesthesiology ; (12): 1237-1239, 2019.
Article in Chinese | WPRIM | ID: wpr-824697

ABSTRACT

Objective To evaluate the effect of penehyelidine hydrochloride(PHCD)on tumor necrosis factor α-induced protein 8-like-2(TIPE2)-Toll-like receptor 4(TLR4)-myeloid differentiation fac-tor 88(MyD88)signaling pathway in a rat model of traumatic acute lung injury(ALI).Methods Thirty SPF healthy male Sprague-Dawley rats,aged 8 weeks,weighing 190-210 g,were divided into 3 groups(n=15 each)by a random number table method: sham operation group(group Sham),traumatic ALI group(group ALI)and group PHCD.ALI was induced by blunt chest trauma in ALI and PHCD groups.PHCD 2 mg/kg was intraperitoneally injected immediately after blunt chest trauma in group PHCD.The rats were sacrificed and lung tissues were removed at 8 h after the model was successfully established for exami-nation of the pathological changes and ultrastructure of lung tissues(with a light microscope or an electron microscope)and for determination of the wet to dry weight ratio(W/D ratio)and expression of TLR4 and MyD88 in lung tissues.Results Compared with group Sham,the W/D ratio was significantly increased,TIPE2 expression was down-regulated,and the expression of TLR4 and MyD88 was up-regulated in ALI and PHCD groups(P<0.05).Compared with group ALI,the W/D ratio was significantly decreased,TIPE2 expression was up-regulated,and the expression of TLR4 and MyD88 was down-regulated(P<0.05),and the pathological changes of lung tissues and ultrastructure were significantly attenuated in group PHCD.Conclusion The mechanism by which PHCD reduces traumatic AIL is related to activating TIPE2-TLR4-MyD88 signaling pathway in rats.

11.
Chinese Journal of Anesthesiology ; (12): 1001-1004, 2019.
Article in Chinese | WPRIM | ID: wpr-824638

ABSTRACT

Objective To evaluate the relationship between tumor necrosis factor-alpha-induced protein 8-like 2 (TIPE2) and caspase-11 during pyroptosis in macrophages of mice.Methods J774A.1 macrophages of mice were divided into 4 groups (n =6 each) using a random number table method:nonspecific siRNA (Scr-siRNA) group (S group),Scr-siRNA plus LPS/ATP group (S+LPS/ATP group),TIPE2-siRNA group (T group) and TIPE2-siRNA plus LPS/ATP group (T+LPS/ATP group).The corresponding siRNA and Lipofectamine2000 transfection reagents were added to each group,and transfection was performed for 24-48 h,and in addition LPS 1.0 μg/ml was then added,cells were incubated for 5 h,then ATP 5.0 mmol/L was added,and cells were incubated for 1 h in S + LPS/ATP and T + LPS/ATP groups.Cells were collected to detect the expression of TIPE2,caspase-11,NOD-like receptor familypyrin domain containing 3 (NLRP3) and caspase-1 (by Western blot).The supernatant was collected for determination of lactic dehydrogenase (LDH) and myeloperoxidase (MPO) activities and concentrations of interleukin-1beta (IL-1β) and IL-18 (by enzyme-linked immunosorbent assay).Results Compared with group S,the expression of TIPE2 was significantly down-regulated,the expression of caspase-11,NLRP3 and caspase-1 was up-regulated,and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group S+LPS/ATP (P<0.05).Compared with group T,the expression of TIPE2 was significantly down-regulated,the expression of caspase-11,NLRP3 and caspase-1 was up-regulated,and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group T+LPS/ATP (P<0.05).Compared with group S+LPS/ATP,the expression of TIPE2 was significantly down-regulated,the expression of caspase-11,NLRP3 and caspase-1 was up-regulated,and and the activities of LDH and MPO and concentrations of IL-1β and IL-18 in supernatant were increased in group T+LPS/ATP (P<0.05).Conclusion TIPE2 inhibits pyroptosis in macrophages through down-regulating the expression of caspase-11 in mice.

12.
Chinese Journal of Anesthesiology ; (12): 1137-1140, 2018.
Article in Chinese | WPRIM | ID: wpr-734639

ABSTRACT

Objective To evaluate the role of protein kinase B∕glycogen synthase kinase-3 beta (Akt∕GSK-3β) signaling pathway in trichostatin-A (TSA)-induced reduction of cerebral ischemia-reperfu-sion ( I∕R) injury in mice. Methods Forty pathogen-free healthy male Balb∕c mice, weighing 18-22 g, were divided into 4 groups ( n=10 each) using a random number table method: sham operation group ( S group), I∕R group, TSA group and TSA plus Akt inhibitor LY294002 group (TL group). Cerebral I∕R was induced by middle cerebral artery occlusion ( 1-h ischemia followed by 24-h reperfusion) . TSA 5 mg∕kg was intraperitoneally injected for 3 consecutive days before establishing the model in TSA group. TSA 5 mg∕kg was intraperitoneally injected for 3 consecutive days before establishing the model, and LY29400215 nmol∕kg was injected via the caudal vein at 30 min before establishing the model. Brain tissues were ob-tained at 24 h of reperfusion for determination of cerebral infarct size ( by TTC ) , activities of superoxidedismutase ( SOD) and reactive oxygen species ( ROS) and malondialdehyde ( MDA) content ( by colorimet-ric assay), cell apoptosis (by TUNEL) and expression of Akt, phosphorylated Akt (p-Akt), GSK-3βand phosphorylated GSK-3β ( p-GSK-3β) . The apoptosis index and ratios of p-Akt∕Akt and p-GSK-3β∕GSK-3β were calculated. Results Compared with S group, the cerebral infarct size was significantly in-creased, the activity of SOD in brain tissues was decreased, the MDA content and ROS activity in brain tissues and apoptosis index were increased, and the ratios of p-Akt∕Akt and p-GSK-3β∕GSK-3β were de-creased in I∕R group ( P<0. 05) . Compared with I∕R group, the cerebral infarct size was significantly de-creased, the activity of SOD in brain tissues was increased, the MDA content and ROS activity in brain tis-sues and apoptosis index were decreased, and the ratios of p-Akt∕Akt and p-GSK-3β∕GSK-3β were de-creased in TSA group ( P<0. 05) . Compared with TSA group, the cerebral infarct size was significantly in-creased, the activity of SOD in brain tissues was decreased, the MDA content and ROS activity in brain tissues and apoptosis index were increased, and the ratios of p-Akt∕Akt and p-GSK-3β∕GSK-3β were de-creased in TL group ( P<0. 05) . Conclusion The mechanism by which TSA attenuates cerebral I∕R injury is related to activating Akt∕GSK-3β signaling pathway in mice.

13.
Article in Chinese | WPRIM | ID: wpr-709876

ABSTRACT

Objective To evaluate the role of classⅠhistone deacetylase (HDAC) in myocardial ischemia-reperfusion (I∕R) injury in diabetic rats and the relationship with adenosine monophosphate-acti- vated protein kinase (AMPK)∕mammalian target of rapamycin (mTOR) signaling pathway. Methods SPF healthy adult male Sprague-Dawley rats, weighing 210-220 g, were used in this study. Type I diabetes mellitus was induced by single intraperitoneal injection of streptozotocin dissolved in citrate buffer 60 mg∕kg, and 8 weeks later the rats with type I diabetes mellitus were used for experiment. Forty-eight diabetic rats were divided into 4 groups (n=12 each) by using a random number table method: sham operation group (group S), myocardial I∕R group (group I∕R), myocardial I∕R plus class I HDAC inhibitor MS-275 group (group I∕R+MS) and myocardial I∕R plus MS-275 plus AMPK inhibitor Compound C group ( group I∕R+MS+CC). Myocardial I∕R was induced by ligation of the left anterior descending branch of the coronary ar-tery for 45 min followed by 180 min of reperfusion in anesthetized rats. In group I∕R+MS, MS-275 10 mg∕kg was intraperitoneally injected once a day for 7 consecutive days, and myocardial I∕R was produced after the end of administration. AMPK inhibitor Compound C 0. 5 mg∕kg was intravenously injected at 30 min before ischemia in group I∕R+MS+CC. Six rats were sacrificed at the end of reperfusion for determina-tion of myocardial infarct size. Another 6 rats were selected at the end of reperfusion and sacrificed for deter-mination of the level of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in serum (by en-zyme-linked immunosorbent assay), expression of AMPK, phosphorylated AMPK ( p-AMPK), mTOR, phosphorylated mTOR (p-mTOR), ubiquitin-binding protein P62 (P62), microtubule-associated protein 1 light chain 3 Ⅰ(LC3 Ⅰ) and LC3Ⅱ in myocardial tissues (by Western blot). The ratios of p-AMPK∕AMPK, p-mTOR∕mTOR and LC3Ⅱ∕Ⅰwere calculated. Results Compared with group S, the myocardial infarct size and levels of serum CK-MB and LDH were significantly increased in I∕R, I∕R+MS and I∕R+M+CC groups, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰwere significantly increased, p-mTOR∕mTOR ratio was decreased, and P62 expression was down-regulated in group I∕R+MS (P<0. 05), and no significant change was found in p-AMPK∕AMPK ratio, p-mTOR∕mTOR ratio, LC3Ⅱ∕Ⅰ ratio or P62 expression in I∕R and I∕R+M+CC groups (P>0. 05). Compared with group I∕R, the myocardial infarct size and levels of serum CK-MB and LDH were significantly decreased, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰwere in-creased, p-mTOR∕mTOR ratio was decreased, and P62 expression was down-regulated in group I∕R+MS (P<0. 05), and no significant change was found in the parameters mentioned above in group I∕R+M+CC (P>0. 05). Compared with group I∕R+MS, the myocardial infarct size and levels of serum CK-MB and LDH were significantly increased, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰ were decreased, p-mTOR∕mTOR ratio was increased, and P62 expression was up-regulated in group I∕R+M+CC ( P<0. 05). Con-clusion Class Ⅰ HDAC is involved in myocardial I∕R injury through enhancing AMPK∕mTOR signaling pathway-regulated level of autophagy in diabetic rats.

14.
Article in Chinese | WPRIM | ID: wpr-805910

ABSTRACT

Objective@#To study the molecular characteristics of norovirus in 4 outbreaks of gastroenteritis in Heilongjiang province in 2016.@*Methods@#Fecal specimens of patients were collected from 4 outbreaks of acute viral gastroenteritis. Real-time PCR was performed to identify the infection with Norovirus (NoV). The NoV genes were amplified and sequenced for the positive samples, followed by performing phylogenetic analysis.@*Results@#There were total 4 outbreaks of viral gastroenteritis caused by NoV. A total of 102 stool specimens were obtained from cases with acute gastroenteritis. NoV was detected in 35 cases including 14 strains of genogroup I NoV and 21 strains of genogroup II NoV. Six genotypes including GII.2, GII.17, GII.Pe, GII.P12/GII.3, GI.6, GI.Pd/GI.3 were detected.@*Conclusions@#NoV was the pathogen causing the gastroenteritis outbreaks in Heilongjiang province, and multigenotype NoV co-circulated in Heilongjiang province.

15.
Article in Chinese | WPRIM | ID: wpr-666707

ABSTRACT

Objective To evaluate the relationship between the mechanism of silent information regulator factor 2-related enzyme 1 (SIRT1)-mediated mitophagy in the myocardium and mitofusin 2 (Mfn2) in diabetic rats.Methods Twenty-four SPF healthy adult male Sprague-Dawley rats,weighing 210-220 g,were allocated into 3 groups (n =8 each) using a random number table:control group (group C),diabetes mellitus group (group DM) and diabetes mellitus plus SIRT1 activator SRT1720 group (group DM+SRT).Diabetes mellitus was induced by intraperitoneal 1% streptozotocin 60 mg/kg and confirmed by blood glucose ≥ 16.7 mmol/L 3 days later.SRT1720 1 mg/kg was injected via the caudal vein for 7 consecutive days in group DM+SRT.The ultrasonic method was used to measure the parameters of heart function including left ventricular end-diastolic volume (LVEDV),left ventricular end-systolic volume (LVESV),left ventricular ejection fraction (LVEF),heart rate (HR),E wave velocity (E),A wave velocity (A) and E/A ratio.Myocardial specimens were obtained for determination of the interaction between SIRT1 and Mfn2 and acetylation of Mfn2 (by co-immuno-precipitation) and expression of SIRT1,Mfn2,microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ),LC3 Ⅰ,Beclin1 and P62 (by Western blot).The ratio LC3 Ⅱ to LC3 Ⅰ (LC3 Ⅱ / Ⅰ ratio) was calculated.Results Compared with group C,LVEDV,LVEF,HR,E and E/A ratio were significantly decreased,A was increased,LC3 Ⅱ / Ⅰ ratio was decreased,the expression of Beclin1,SIRT1 and Mfn2 was down-regulated,the expression of P62 was up-regulated,and the interaction between SIRT1 and Mfn2 was decreased in group DM (P<0.05).Compared with group DM,LVEDV,LVEF,E and E/A ratio were significantly increased,A was decreased,LC3 Ⅱ / Ⅰ ratio was increased,the expression of Beclin1 and SIRT1 was up-regulated,the expression of P62 was down-regulated,the interaction between SIRT1 and Mfn2 was increased,and the acetylation of Mfn2 was decreased in group DM+SRT (P<0.05).Conclusion The mechanism by which SIRT1 mediates mitophagy in the myocardium is related to SIRT1-induced deacetylation of Mfn2 in diabetic rats.

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Article in Chinese | WPRIM | ID: wpr-489372

ABSTRACT

Objective To evaluate the effects of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway on the brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Pathogen-free male Sprague-Dawley rats,weighing 200-220 g,were used in this study.Diabetes mellitus was induced by intraperitoneal 1% streptozotocin 60 mg/kg and confirmed by blood glucose level ≥ 16.7 mmol/L 3 days later.Twenty-four rats with diabetes mellitus were randomly allocated into 3 groups (n =8 each) using a random number table:sham operation group (group S),I/R group,and myocardial I/R + AG490 (JAK inhibitor) group (group ⅠA).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min,followed by 120 min of reperfusion in the rats anesthetized with pentobarbital sodium.AG490 3 mg/kg was injected intravenously at 20 min before reperfusion in group IA.The rats were sacrificed at 120 min of reperfusion,and the brains were removed for determination of caspase-3 and nuclear factor kappa B (NF-κB) activities (using colorimetric method),cell apoptosis (by TUNEL),and expression of interleukin-1 (IL-1),IL-6,IL-8,Bax,Bcl-2,cytochrome C (Cyt c),phosphorylated JAK2 (p-JAK2),and phosphorylated STAT3 (p-STAT3) (by Western blot).Apoptosis index was calculated.Results Compared with group S,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly up-regulated,the expression of Bcl-2 was down-regulated,and NF-κB and caspase-3 activities and apoptosis index were increased in I/R and IA groups (P<0.05).Compared with group I/R,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly down-regulated,the expression of Bcl-2 was up-regulated,and NF-κB and caspase-3 activities and apoptosis index were decreased in group IA (P<0.05).Conclusion Inflammatory responses mediated by JAK2/STAT3 signaling pathway are involved in the brain injury induced by myocardial I/R in diabetic rats.

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Herald of Medicine ; (12): 789-792, 2016.
Article in Chinese | WPRIM | ID: wpr-492953

ABSTRACT

Objective To evaluate the effects of ulinastatin on perioperative inflammatory response during cardiopulmonary bypass. Methods Comprehensive search of PubMed,EMbase,the Cochrane Library,CECDB,CQVIP,CNKI databases was conducted for randomized controlled trials(RCTs) published from January 1994 to June 2014.The included studies were evaluated strictly and the extracted data were analyzed by RevMan 5.2. Results A total of 7 RCTs including 335 patients were included,and 154 patients were in the experimental group,while 181 patients were in the control group.In the experimental group, patients were given Ulinastatin during surgery. System evaluation results show that, the concentration of TNF-α [ SMD (95%CI) were -3.48(-4.64,-2.31)] and IL-6 [SMD(95%CI) were -3.04(-4.54,-1.54)] in experimental group at 1 h after weaning from CPB were significantly lower than those in control group. Conclusion Ulinastatin used perioperatively in cardiopulmonary bypass can significantly reduce postoperative inflammation.

18.
Herald of Medicine ; (12): 455-458, 2015.
Article in Chinese | WPRIM | ID: wpr-464679

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Objective To investigate the effects of huaier granules on invasion and metastasis of colorectal cancer SW480 cells in vitro, and explore the basic mechanism. Methods The appropriate concentration and duration of huaier granules promoting SW480 cell apoptosis were determined by SubG1 method. Wound healing assay and transwell assay were used to observe the effect of huaier granules on SW480 cell invasion and metastasis. The changes of E-cadherin, twist, snail and vimentin at protein and mRNA levels were examined by Western blotting and Real-Time PCR. Results After treatment with huaier granules at 3. 0 g·L-1 for 36 h, apoptosis of SW480 cells was most significant, and wound healing assay revealed that relative mobility was (31. 36±2. 39)%, compared with (61. 11±1. 09)% in control group (P<0. 01). Number of invaded cells per field of view was (129±12) in treatment group and (354±20) in control group (P<0. 01). After treatment with huaier granules at 3. 0 g·L-1 for 36 h, protein and mRNA levels of E-cadherin were increased, while those of twist, snail and vimentin were decreased. Conclusion Huaier granules can inhibit invasion and metastasis of colorectal cancer SW480 cells in vitro through effectively depressing epithelial-mesenchymal transition.

19.
Chinese Journal of Anesthesiology ; (12): 1138-1141, 2015.
Article in Chinese | WPRIM | ID: wpr-483311

ABSTRACT

Objective To investigate the effects of penehyclidine hydrochloride on Fas/FasL expression during acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male SPF Sprague-Dawley rats, aged 8 weeks, weighing 245-275 g, were randomly assigned into 3 equal groups using a random number table: sham operation group (group Sham) , blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloric group (group PHCD).The model of acute lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until mean arterial pressure was decreased to 35-45 mmHg within 15 min, and maintained at this level for 60 min, followed by resuscitation.In PHCD group, PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established, the rats were sacrificed, the lungs were then removed for microscopic examination of pathologic changes and for determination of Fas, FasL and caspase-8 expression, and interleukin-6 (IL-6) and IL-1β contents in lung tissues.Apoptotic index was calculated.Results Compared with group Sham, the expression of Fas, FasL and caspase-8 was significantly up-regulated, and AI and contents of IL-6 and IL-1β were increased in THSR and PHCD groups (P<O.05).Compared with group THSR, the expression of Fas, FasL and caspase-8 was significantly down-regulated,and AI and contents of IL-6 and IL-1β were decreased in group PHCD (P<0.05).The pathologic changes of lungs were significantly reduced in group PHCD compared with group THSR.Conclusion The mechanism by which penehyclidine hydrochloride inhibits lung cell apoptosis induced by blunt chest trauma-HSR is associated with inhibition of Fas/FasL expression in rats.

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Article in Chinese | WPRIM | ID: wpr-482979

ABSTRACT

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

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