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1.
Rev. colomb. anestesiol ; 50(1): e300, Jan.-Mar. 2022. tab, graf
Article in English | LILACS-Express | LILACS | ID: biblio-1360948

ABSTRACT

Abstract Adult In-hospital Cardiac Arrest (IHCA) is defined as the loss of circulation of an in-patient. Following high-quality cardiopulmonary resuscitation (CPR), if the return of spontaneous circulation (ROSC) is achieved, the post-cardiac arrest syndrome develops (PCAS). This review is intended to discuss the current diagnosis and treatment of PCAS. To approach this topic, a bibliography search was conducted through direct digital access to the scientific literature published in English and Spanish between 2014 and 2020, in MedLine, SciELO, Embase and Cochrane. This search resulted in 248 articles from which original articles, systematic reviews, meta-analyses and clinical practice guidelines were selected for a total of 56 documents. The etiologies may be divided into 56% of in-hospital cardiac, and 44% of non-cardiac arrests. The incidence of this physiological collapse is up to 1.6 cases/1,000 patients admitted, and its frequency is higher in the intensive care units (ICU), with an overall survival rate of 13% at one year. The primary components of PCAS are brain injury, myocardial dysfunction and the persistence of the precipitating pathology. The mainstays for managing PCAS are the prevention of cardiac arrest, ventilation support, control of peri-cardiac arrest arrythmias, and interventions to optimize neurologic recovery. A knowledgeable healthcare staff in PCAS results in improved patient survival and future quality of life. Finally, there is clear need to do further research in the Latin American Population.


Resumen El paro cardiaco intrahospitalario en el adulto (IHCA) se define como el cese de circulación ocurrido dentro de las instalaciones hospitalarias. Después de la reanimación cardiopulmonar (RCP) de alta calidad, si se logra el retorno de circulación espontánea (ROSC), aparece entonces el síndrome posparo cardiaco (SPPC). En esta revisión se pretende presentar el estado actual del diagnóstico y tratamiento del SPPC. Para abordar este tema, se realizó una búsqueda bibliográfica mediante la consulta digital directa de la literatura científica publicada entre 2014 y 2020 en inglés y español recogida en las bases de datos MedLine, SciELO, Embase y Cochrane. La búsqueda inicial arrojó 248 artículos, de los cuales se eligieron artículos originales, revisiones sistemáticas, metaanálisis y guías de práctica clínica, para una selección final de 56 documentos. Las etiologías del paro cardiaco intrahospitalario se pueden dividir en cardiacas y no cardiacas, en el 56 % y 44 %, respectivamente. El colapso fisiológico tiene incidencias de hasta 1,6 casos/1.000 pacientes admitidos, y es más frecuente en las unidades de cuidado intensivo (UCI), con una tasa de supervivencia general de 1 año del 13 %. Los componentes principales del SPPC son la lesión cerebral, la disfunción miocárdica y la persistencia de la patología precipitante. Los pilares del manejo del SPPC son la prevención del paro cardiaco, soporte ventilatorio, control de arritmias periparo cardiaco y las intervenciones para optimizar la recuperación neurológica. El conocimiento del SPPC por parte del personal de la salud ofrece mejor sobrevida y futura calidad de vida a los pacientes. Finalmente, se resalta la clara necesidad de ahondar en mayores investigaciones en la población latinoamericana.

2.
Rev. Assoc. Med. Bras. (1992) ; 68(1): 87-93, Jan. 2022. tab, graf
Article in English | LILACS | ID: biblio-1360707

ABSTRACT

SUMMARY OBJECTIVE: The aim of this study was to evaluate the hepatoprotective effect and mechanism of action of artichoke leaf extract in hepatic ischemia/reperfusion injury. METHODS: Rats were divided into three groups such as sham, control, and artichoke leaf extract groups. Antioxidant enzyme activities and biochemical parameters were examined from the tissue and serum obtained from the subjects. Histopathological findings were scored semiquantitatively. RESULTS: Statistically, the antioxidant activity was highest in the artichoke leaf extract group, the difference in biochemical parameters and C-reactive protein was significant compared with the control group, and the histopathological positive effects were found to be significantly higher. CONCLUSIONS: As a result, artichoke leaf extract had a hepatoprotective effect and that this effect was related to the antioxidant and anti-inflammatory effects of artichoke.


Subject(s)
Animals , Rats , Reperfusion Injury/prevention & control , Reperfusion Injury/drug therapy , Cynara scolymus , Plant Extracts/therapeutic use , Plant Extracts/pharmacology , Liver , Antioxidants/metabolism , Antioxidants/therapeutic use , Antioxidants/pharmacology
3.
Organ Transplantation ; (6): 277-2022.
Article in Chinese | WPRIM | ID: wpr-920861

ABSTRACT

Mitochondria is one of the important organelles, which is composed of outer mitochondrial membrane and inner mitochondrial membrane. Mitochondrial structure and function are regulated by mitochondrial dynamics. Mitochondrial fusion- and fission-related proteins may participate in the process of mitochondrial fusion and fission, mediate mitochondrial dynamics, thereby regulating cell structure, function and energy metabolism. Mitofusin (MFN) 2, a protein located on the outer mitochondrial membrane of mammalian, has guanosine triphosphatase activity, which may mediate mitochondrial fusion, participate in mitophagy, formation of mitochondria-associated endoplasmic reticulum membrane and apoptosis, and significantly affect the incidence and development of ischemia-reperfusion injury (IRI). In this article, the structure, regulation, function of MFN2 and its role in IRI were reviewed, and the relationship between MFN2 and IRI and underlying mechanism were investigated, aiming to provide novel targets and ideas for the prevention and treatment of IRI.

4.
Article in English | WPRIM | ID: wpr-920349

ABSTRACT

@#BACKGROUND: We aimed to investigate the gene expression of myocardial ischemia/reperfusion injury (MIRI) in patients with acute ST-elevation myocardial infarction (STEMI) using stress and toxicity pathway gene chip technology and try to determine the underlying mechanism. METHODS: The mononuclear cells were separated by ficoll centrifugation, and plasma total antioxidant capacity (T-AOC) was determined by the ferric reducing ability of plasma (FRAP) assay. The expression of toxic oxidative stress genes was determined and verified by oligo gene chip and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, gene ontology (GO) enrichment analysis was performed on DAVID website to analyze the potential mechanism further. RESULTS: The total numbers of white blood cells (WBC) and neutrophils (N) in the peripheral blood of STEMI patients (the AMI group) were significantly higher than those in the control group (WBC: 11.67±4.85 ×109/L vs. 6.41±0.72 ×109/L, P<0.05; N: 9.27±4.75 ×109/L vs. 3.89±0.81 ×109/ L, P<0.05), and WBCs were significantly associated with creatine kinase-myocardial band (CK-MB) on the first day (Y=8.945+0.018X, P<0.05). In addition, the T-AOC was significantly lower in the AMI group comparing to the control group (12.80±1.79 U/mL vs. 20.48±2.55 U/mL, P<0.05). According to the gene analysis, eight up-regulated differentially expressed genes (DEGs) included GADD45A, PRDX2, HSPD1, DNAJB1, DNAJB2, RAD50, TNFSF6, and TRADD. Four down-regulated DEGs contained CCNG1, CAT, CYP1A1, and ATM. TNFSF6 and CYP1A1 were detected by polymerase chain reaction (PCR) to verify the expression at different time points, and the results showed that TNFSF6 was up-regulated and CYP1A1 was down-regulated as the total expression. GO and kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis suggested that the oxidative stress genes mediate MIRI via various ways such as unfolded protein response (UPR) and apoptosis. CONCLUSIONS: WBCs, especially neutrophils, were the critical cells that mediating reperfusion injury. MIRI was regulated by various genes, including oxidative metabolic stress, heat shock, DNA damage and repair, and apoptosis-related genes. The underlying pathway may be associated with UPR and apoptosis, which may be the novel therapeutic target.

5.
Acta Pharmaceutica Sinica ; (12): 409-418, 2022.
Article in Chinese | WPRIM | ID: wpr-922916

ABSTRACT

We investigated the ability of Dracocephalum moldavica (EPDM) flavonoids to protect human brain microvascular endothelial cells (HBMECs) from necroptosis induced by ischemia-reperfusion injury. To mimic the process of cerebral ischemia-reperfusion injury, a necroptosis model was established by treatment with the pan-cysteine aspartic acid protease (caspase) inhibitor Z-VAD-FMK combined with oxygen-glucose deprivation/re-oxygenation (OGD/R) injury using HBMECs. Cell proliferation and cytotoxicity (cell counting kit-8, CCK-8) was used to measure cell viability. A Hoechst33342/PI fluorescent double-staining method was exploited to determine the rate of cell necroptosis. A commercial kit was used to detect lactate dehydrogenase in the cell culture supernate. DCFH-DA probes, calcein AM and JC-1 probes were used to measure changes in ROS production, mitochondrial membrane permeability transformation pore (MPTP) opening and mitochondrial membrane potential (MMP), respectively. Enzyme-linked immunosorbent assay (ELISA) kits were chosen to detect the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Western blotting was used to detect necroptosis-related proteins. The results show that relative to control group, Z-VAD-FMK combined with OGD/R injury reduced cell viability, increased the necroptosis rate and the levels of LDH and ROS in HBMECs. The MPTP of the model group cells opened and the MMP reduced. TNF-α, IL-1β, and IL-6 levels were significantly elevated. Furthermore, the expression of receptor-interacting protein kinase 3 (RIP3) and mitochondrial phosphoglycerate mutase 5 (PGAM5) was significantly increased, accompanied by an increase of phosphorylated mixed-lineage kinase domain-like protein (p-MLKL)/MLKL. EPDM partially reversed the changes of the above-mentioned factors in HBMECs induced by Z-VAD-FMK plus OGD/R injury. These results indicate that EPDM may protect HBMECs from cerebral ischemia-reperfusion injury by inhibiting the RIP3/MLKL/PGAM5 pathway and MPTP opening to maintain mitochondrial function, thereby providing a scientific basis for the use of EPDM in the treatment of cerebral ischemia-related diseases.

6.
Organ Transplantation ; (6): 126-2022.
Article in Chinese | WPRIM | ID: wpr-907043

ABSTRACT

Common marginal donor liver mainly consists of fatty donor liver, elderly donor liver, small volume donor liver and liver graft from donation after cardiac death (DCD), etc. The application of marginal donor liver may resolve the severe shortage of donor liver to certain extent. Nevertheless, marginal donor liver yields a higher risk of ischemia-reperfusion injury (IRI) and causes more severe IRI than normal donor liver, which is a main cause for the failure of transplantation. In addition, oxidative stress is a major risk factor causing IRI of marginal donor liver. Therefore, how to mitigate oxidative stress and alleviate IRI of marginal donor liver has become a hot spot in clinical practice. Reactive oxygen species (ROS)-mediated oxidative stress occurs throughout the whole process of IRI. In this article, the role of oxidative stress in IRI of marginal donor liver transplantation and the ROS-targeted prevention and treatment were reviewed, aiming to provide reference for clinical practice.

7.
Organ Transplantation ; (6): 88-2022.
Article in Chinese | WPRIM | ID: wpr-907038

ABSTRACT

Objective To evaluate the effect of high mobility group box 1 (HMGB1)/ cysteinyl aspartate specific proteinase (Caspase)-1/Gasdermin D (GSDMD) signaling axis-mediated hepatocyte pyroptosis on liver ischemia-reperfusion injury (IRI). Methods C57BL/6 mice were randomly divided into the sham operation group (Sham group), IRI 2 h group, IRI 6 h group, IRI 12 h group, glycyrrhizic acid (GA)+Sham group and GA+IRI 12 h group (n=8 in each group). AML12 cells were evenly divided into the Sham group, IRI 12 h group, GA+Sham group and GA+IRI 12 h group. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin (IL)-1β and IL-6 in each group were detected by enzyme-linked immune absorbent assay(ELISA). The messenger ribonucleic acid (mRNA) levels of IL-1β and IL-6 were detected by reverse transcription polymerase chain reaction(RT-PCR). The pathological score of liver ischemia and cell apoptosis were compared among all groups. The expression level of HMGB1 in the liver tissues of each group was determined by immunohistochemistry. The expression levels of HMGB1, Caspase-1 and GSDMD proteins in the mouse liver tissues and AML12 cells were measured by Western blot. Results Compared with the Sham group, the serum levels of ALT, AST, IL-1β and IL-6 and the relative expression levels of IL-1β and IL-6 mRNA in the liver tissues were all significantly up-regulated after IRI in each group (all P < 0.05), and showed significant time-dependent pattern along with the prolongation of reperfusion time. Compared with the Sham group, the pathological score of hepatic ischemia and the apoptosis rate of hepatocytes were significantly increased after IRI in each group (all P < 0.05). Immunohistochemical results showed that the expression level of HMGB1 in the liver tissues was significantly up-regulated after IRI, which showed an increasing trend along with the prolongation within the period of 2-12 h. Western blot showed that compared with the Sham group, the relative expression levels of HMGB1, Caspase-1 and GSDMD proteins in vivo and in vitro were up-regulated in the IRI 12 h group. The relative expression level of HMGB1 protein was significantly up-regulated, whereas those of Caspase-1 and GSDMD proteins were significantly down-regulated in the GA+IRI 12 h group compared with those in the IRI 12 h group (all P < 0.05). Conclusions Hepatocytes probably activate the Caspase-1/GSDMD signaling pathway by releasing HMGB1, thereby triggering hepatocyte pyroptosis and leading to liver IRI. Inhibition of extracellular release of HMGB1 by GA may mitigate liver IRI.

8.
Organ Transplantation ; (6): 74-2022.
Article in Chinese | WPRIM | ID: wpr-907036

ABSTRACT

Objective To evaluate the predictive values of serum neutrophil gelatinase-associated lipocalin (NGAL), urine NGAL, serum cystatin C (Cys-C) and serum creatinine (Scr) for early delayed graft function (DGF) in kidney transplant recipients. Methods Clinical data, blood and urine samples of 159 kidney transplant recipients were collected. All recipients were divided into the DGF group (n=42) and immediate graft function (IGF) group (n=117) according to the incidence of DGF. Clinical data of all recipients were analyzed. The changes of serum NGAL, urine NGAL, Cys-C and Scr levels were statistically compared between two groups. The predictive values of different markers for early DGF were assessed. Results Among 159 kidney transplant recipients, DGF occurred in 42 cases with an incidence rate of 26.4%. There were statistically significant differences in donor age, cold ischemia time of donor kidney and complement-dependent cytoxicity (CDC) between the two groups(all P < 0.05). Within postoperative 2 weeks, the serum NGAL levels in the DGF group were higher than those in the IGF group (all P < 0.05). The Cys-C, Scr and urine NGAL levels in the DGF group were higher compared with those in the IGF group within 3 weeks after kidney transplantation(all P < 0.001). Serum NGAL, urine NGAL, Cys-C and Scr levels had certain predictive values for early DGF in kidney transplant recipients. Cys-C yielded the highest predictive value with a cut-off value of 4.73 mg/L, sensitivity of 0.833, specificity of 0.812 and area under the curve (AUC) of 0.895. Conclusions Cys-C has higher predictive value for early DGF in kidney transplant recipients compared with serum NGAL, urine NGAL and Scr.

9.
Arq. bras. cardiol ; 117(2): 290-297, ago. 2021. tab, graf
Article in English, Portuguese | LILACS | ID: biblio-1339163

ABSTRACT

Resumo Fundamento: O núcleo do trato solitário (NTS) é uma área do cérebro que desempenha um papel fundamental na regulação renal e cardiovascular através dos impulsos dos barorreceptores. Objetivos: O objetivo deste estudo foi avaliar o efeito da Naringina (NAR) e trimetazidina (TMZ), isoladamente e combinadas, na atividade elétrica do NTS e na sensibilidade barorreflexa (SBR) na lesão de isquemia e reperfusão (I/R) renal. Métodos: Foram utilizados quarenta ratos machos Sprague-Dawley (200-250 g), alocados em 5 grupos com 8 ratos cada. Grupos: 1) Sham; 2) I/R; 3) TMZ 5 mg/kg; 4) NAR 100 mg/kg; e 5) TMZ5 + NAR100. A veia femoral esquerda foi canulada para infundir a solução salina ou droga e avaliar a SBR. A I/R foi induzida por oclusão dos pedículos renais por 45 min, seguida de reperfusão de 4 horas. O eletroencefalograma local do NTS foi registrado antes, durante a isquemia e durante a reperfusão. A fenilefrina foi injetada por via intravenosa para avaliar a SBR ao final do tempo de reperfusão. Os dados foram analisados por ANOVA de duas vias com medidas repetidas seguida pelo teste post hoc de Tukey. Um valor de p<0,05 foi considerado como significativo. Resultados: As ondas elétricas do NTS não se alteraram durante o tempo de isquemia, mas diminuíram significativamente durante todos os tempos de reperfusão. A atividade elétrica do NTS e a SBR foram reduzidas drasticamente em ratos com lesão I/R; no entanto, a administração de NAR e TMZ, isoladamente e combinadas, melhorou significativamente essas alterações em ratos com lesão I/R. Conclusões: Os resultados mostraram que a lesão de I/R leva à redução da atividade elétrica da SBR e do NTS, e pode haver uma ligação entre a I/R e a diminuição da SBR. Além disso, a NAR e a TMZ são agentes promissores para tratar complicações de I/R.


Abstract Background: Nucleus tractus solitarius (NTS) is a brain area that plays a key role in kidney and cardiovascular regulation via baroreceptors impulses. Objectives: The aim of this study was to evaluate the effect of naringin (NAR) and trimetazidine (TMZ) alone and their combination on NTS electrical activity and baroreceptor sensitivity (BRS) in renal ischemia- reperfusion (I/R) injury. Methods: Forty male Sprague-Dawley rats (200- 250 g) were allocated into 5 groups with 8 in each. 1) Sham; 2) I/R; 3) TMZ 5 mg/kg; 4) NAR 100 mg/kg; and 5) TMZ5+ NAR100. The left femoral vein was cannulated to infuse saline solution or drug and the BRS was evaluated. I/R was induced by occlusion of renal pedicles for 45 min, followed by 4 hours of reperfusion. The NTS local electroencephalogram (EEG) was recorded before, during ischemia and throughout the reperfusion. Phenylephrine was injected intravenously to evaluate BRS at the end of reperfusion time. The data were analyzed by two-way repeated measurement ANOVA followed by Tukey's post hoc test. A p-value <0.05 was considered significant. Results: NTS electrical waves did not change during ischemia time, while they significantly decreased during the entire reperfusion time. NTS electrical activity and BRS dramatically reduced in rats with I/R injury; however, administration of NAR, TMZ alone or their combination significantly improved these changes in rats with I/R injury. Conclusions: The results showed that I/R injury leads to reduced BRS and NTS electrical activity and there may be an association between I/R and decreased BRS. In addition, NAR and TMZ are promising agents to treat I/R complications.


Subject(s)
Animals , Male , Rats , Trimetazidine/pharmacology , Reperfusion Injury/prevention & control , Reperfusion Injury/drug therapy , Rats, Sprague-Dawley , Solitary Nucleus , Baroreflex , Flavanones , Kidney
10.
Rev. cuba. ortop. traumatol ; 35(1): e341, 2021.
Article in Spanish | LILACS, CUMED | ID: biblio-1289549

ABSTRACT

Introducción: El torniquete es ampliamente usado en la cirugía ortopédica y traumatológica con el objetivo de disminuir las pérdidas sanguíneas intraoperatorias y mejorar la visibilidad de las estructuras anatómicas, aunque su empleo es controversial. Objetivo: Describir las aplicaciones prácticas y las limitaciones del torniquete en la cirugía ortopédica y traumatológica. Método: Se realizó una revisión no sistemática de la literatura en bases de datos científicas como Cochrane Database of Systematic Reviews, Pubmed/Medline, EMBASE, Scopus, Web of Science, EBSCOhost, ScienceDirect, OVID y el buscador académico Google Scholar, en el mes de septiembre de 2020. Conclusiones: Aunque el torniquete es ampliamente utilizado durante la cirugía ortopédica y traumatológica, debido a que contribuye a reducir las pérdidas hemáticas intraoperatorias, se ha demostrado su efecto en el aumento de las pérdidas sanguíneas totales, así como su asociación con dolor perioperatorio, pérdida de la fuerza muscular del miembro, lesiones de nervios periféricos, trombosis venosa profunda y daño a órganos a distancia por el fenómeno de isquemia-reperfusión(AU)


Introduction: Although controversial, tourniquets are widely used in orthopedic and trauma surgery with the aim of reducing intraoperative blood losses and improving the visibility of anatomical structures. Objective: To describe the practical applications and limitations of tourniquets in orthopedic and trauma surgery. Method: A non-systematic review of the literature was carried out, in scientific databases such as Cochrane Database of Systematic Reviews, Pubmed / Medline, EMBASE, Scopus, Web of Science, EBSCOhost, ScienceDirect, OVID and the academic search engine Google Scholar, in the month of September 2020. Conclusions: Although tourniquets are widely used during orthopedic and trauma surgery, since they contribute to reducing intraoperative blood loss, the effect on increasing total blood loss has been demonstrated, as well as the association with perioperative pain, blood loss, limb muscle strength, peripheral nerve injuries, deep vein thrombosis and damage to distant organs due to the ischemia-reperfusion phenomenon(AU)


Subject(s)
Humans , Tourniquets/classification , Orthopedics , Traumatology
11.
Article in English | WPRIM | ID: wpr-922098

ABSTRACT

OBJECTIVE@#To investigate the synergistic effect of Naoxintong Capsule (NXTC, ) and Guhong Injection (GHI, ) on cerebral ischemia-reperfusion (I/R) injury.@*METHODS@#Forty-eight Sprague-Dawley rats were divided into 6 groups: control group, oxygen and glucose deprivation (OGD) group, nimodipine group (9.375 mg/kg), NXTC group (0.5 g/kg), GHI group (5 mL/kg) and NXTC+GHI group (0.5 g/kg NXTC+5 mL/kg GHI), after the onset of reperfusion and once per day for the following 7 days. Blood was collected 1 h after final administration, and the sera were collected. Cultured primary rat brain microvascular endothelial cells (rBMECs) were subjected to OGD to establish a cell injury model. Untreated rBMECs were used as blank control. The cell counting kit-8 assay was used to assess cell viability using the sera. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were assessed using an enzyme-linked immunosorbent assay. Apoptosis was evaluated after Hoechst33342 staining using fluorescence microscopy and flow cytometry. JC-1 staining was performed to assess changes in mitochondrial membrane potential.@*RESULTS@#Statistical analysis indicated that more than 95% of the cells were rBMECs. Compared with the OGD group, the cellular morphology of the all drug delivery groups improved. In particular, the combined drug group had the most significant effect. Compared with the OGD group, all drug intervention groups induced a decrease in the apoptotic rate of rBMECs, increased the SOD levels, and decreased the MDA levels (all P<0.01). Compared with the mono-therapy groups, the NXTC+GHI group exhibited a significant improvement in the number of apoptotic rBMECs (P<0.01). All drug intervention groups showed different degrees of increase in membrane potential, and the NXTC+GHI group was higher than the NXTC or GHI group (P<0.01).@*CONCLUSION@#The combinationa application of NXTC and GHI on cerebral I/R injury clearly resulted in protective benefits.


Subject(s)
Animals , Apoptosis , Brain , Brain Ischemia/drug therapy , Drugs, Chinese Herbal , Endothelial Cells , Glutamine/analogs & derivatives , Plant Extracts , Rats , Rats, Sprague-Dawley , Reperfusion Injury/drug therapy
12.
Article in Chinese | WPRIM | ID: wpr-911692

ABSTRACT

Objective:To explore whether hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) preconditioning can relieve inflammation, reduce cell apoptosis and alleviate renal ischemia-reperfusion injury in mice.Methods:Male C57BL/6 mice were randomly divided into three groups of sham operation (sham), ischemia reperfusion injury (IRI) and IRI+ HIF-PHI ( n=6 each). In IRI+ HIF-PHI group, mice received an intragastric dose of roxadustat (20 mg/kg) every other day one week before. After renal IRI modeling, serum creatinine (SCr) level was monitored and hematoxylin-eosin (HE) staining employed for observing the pathological changes of renal tissue and scoring injury degree. Apoptosis of renal tubular epithelial cells was assessed by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). Reverse transcription-polymerase chain reaction (RT-PCR) was utilized for detecting the mRNA expressions of HIF-1α, TNF-α and IL-1β in renal tissues. Immunofluorescence and immunohistochemistry were employed for detecting the expressions of hypoxia-inducing factor 1α (HIF-1α), inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). Results:As compared with IRI group, SCr level declined markedly in IRI+ HIF-PHI group ( P<0.01), renal tissue injury improved markedly, semi-quantitative score of renal tubule injury dropped ( P<0.01), apoptotic cells decreased ( P<0.01) and the expression levels of TNF-α and IL-1β declined ( P<0.05). Compared with sham group, the mRNA expression of HIF-1α was not significantly elevated in IRI group ( P>0.05). Immunofluorescence showed that the expression of HIF-1α in medulla of renal tissues was up-regulated in IRI group, but not markedly in cortex. While the mRNA expression of HIF-1α was markedly up-regulated after a pretreatment of HIF-PHI ( P<0.05), the expression spiked markedly in renal cortex, but was weaker in medulla than that in IRI group. Conclusions:HIF-PHI can boost the expression level of HIF-1α, reduce the expression of inflammatory factors, relieve the inflammatory response, reduce cell apoptosis, improve renal function and alleviate renal ischemia reperfusion injury.

13.
Article in Chinese | WPRIM | ID: wpr-911685

ABSTRACT

Objective:To explore the protective effect of puerarin on hypoxia/reoxygenation (H/R)-induced acute kidney injury(AKI)in vitro.Methods:HK-2 cells were treated with H/R for simulating ischemia reperfusion injury(IRI)in vivo. The experimental groups included control group, H/R treatment group(0/6/12/24 h), H/R 24 h + puerarin treatment group(puerarin, Pue), H/R 24 h + Pue+ 3-methyladenine(3-MA)treatment group and H/R 24 h+ 3-MA treatment group. Immunoblotting was employed for detecting the expression changes of autophagy-related proteins, CCK-8 for examining cell proliferation, electron microscopy for observing autophagosome formation and TUNEL for detecting apoptosis.Results:As compared with control group, the expression of LC3-II rose in H/R 24 h group, the expression of autophagy marker P62 declined, count of autophagosome increased, cell viability decreased and cellular inflammation occurred. Puerarin had similar effects to 3-MA. As compared with H/R 24 h group, puerarin could reverse the changes in the expression levels of LC3 and P62 induced by H/R( P<0.05). There were greater cell viability, reduced autophagosome count and lessened cell apoptosis( P<0.05). At the same time, protein expression levels of HMGB1, TLR4 and NF-κB dropped( P<0.05). Conclusions:Puerarin suppresses autophagy through HMGB1/TLR4/NF-κB axis for lessening ischemia-reperfusion injury an in vitro model.

14.
Article in Chinese | WPRIM | ID: wpr-911638

ABSTRACT

Objective:To develop an ex vivo normothermic mechanical perfusion(NMP)and compare the effect of different portal perfusion pressures on attenuating hepatic injury from donor after cardiac death(DCD).Methods:All rat livers were subjected to in situ warm ischemia for 30 min after cardiac attest and thereafter stored for 8 h under cold preservation. Six livers were harvested and regarded as static cold storage(group CS, n=6). In experimental group, liver received an ex vivo dual NMP with oxygenated perfusion via hepatic artery for 2 h after cold storage. Hepatic injury was assessed and compared from perfused livers with full portal vein pressure(group M1, n=6)and low portal vein pressure(group M2, n=6). The evaluation parameters included perfusion flow, liver enzymes of perfusate, pathological changes by hematoxylin-eosin staining, Suzuki histological criteria, expression of activation markers of polymorphonuclear neutrophils and macrophages, myeloperoxidase (MPO)and CD68 by immunohistochemistry, level of malondialdehyde(MDA)and activity of superoxide dismutase(SOD). Results:In experimental group during NMP, perfusion flows tended to increase when portal pressures were stabilized in groups M1 and M2.Perfusion flow during NMP 60~120 min was significantly higher than during NMP 0~20 min.After NMP with full portal pressure, hepatic sinusoidal congestion, hepatocyte necrosis, steatosis and Suzuki criteria were lower in group M1 than those in group CS( P<0.05). Compared with group M1, lower hepatic injury was characterized with a lower change of liver enzymes in perfusate( P<0.05), a better histological evaluation( P<0.05), a lower level of MDA and a higher activity of SOD( P<0.05), lower expressions of CD68 and MPO ( P<0.05)and lower levels of TNF-α and IL-6( P<0.05)in perfused liver. Conclusions:The ex vivo dual NMP with oxygenated perfusion via hepatic artery mimics liver perfusion under the physiological conditions.NMP with a lower portal pressure can attenuate hepatic ischemia-reperfusion injury and confer a better protection against liver damage from DCD.

15.
Chinese Journal of Urology ; (12): 554-558, 2021.
Article in Chinese | WPRIM | ID: wpr-911071

ABSTRACT

Renal ischemia-reperfusion injury often occurs during operations that need to block the blood supply of the kidneys. It is an important pathophysiological process that affects the recovery of kidney function and causes acute renal failure. Activated NLRP3 inflammasome can mediate the maturation and release of a variety of pro-inflammatory factors, and participate in the inflammatory response in renal ischemia-reperfusion injury, thereby regulating body inflammation and related cell functions. This article summarized how NLRP3 inflammasome mediated the occurrence of inflammation in renal ischemia reperfusion injury, and further provied a new basis for the prevention and treatment of renal ischemia-reperfusion injury.

16.
Article in Chinese | WPRIM | ID: wpr-909605

ABSTRACT

The morbidity and mortality of cardiovascular diseases are very high, which has attracted more and more attention all over the world. Common treatment methods for clinical treatment of acute myocardial infarction include direct percutaneous coronary intervention and coronary artery bypass grafting, which can quickly restore blocked coronary blood flow and reduce the infarct size. However, the inevitable ischemia/reperfusion injury will occur during the recovery of coronary blood flow, its pathological mechanism is complicated, and the Western medicine countermeasures are very limited. Among the current drugs for the treatment of cardiovascular diseases, traditional Chinese medicine has become a research hotspot due to its multiple targets, safety, and low side effects. Ginger is the fresh rhizome of Zingiber offici?nale Rosc., a perennial herbaceous plant in the ginger family. It is a dual-purpose resource of medicine and food. Ginger has the functions of relieving the appearance and dispelling cold, warming up and relieving vomiting, resolving phlegm and relieving cough, and relieving fish and crab poison. The chemical components of ginger mainly include volatile oil, gingerol, diphenylheptane, etc.. Among them, 6-gingerol, as the main active component of gingerols, has obvious phar?macological effects in myocardial protection, anti-oxidation, anti-inflammatory, etc.. Studies have shown that 6-gingerol protects myocardium mainly through anti-oxidative stress, anti-inflammatory, inhibiting cell apoptosis, and preventing cal?cium influx. ① Anti-oxidative stress: oxidative stress is a state where oxidation and anti-oxidation in the body are out of balance, and it is also an important factor leading to myocardial damage. Many studies have confirmed that 6-gingerol has an antioxidant effect, and it is considered a natural antioxidant. 6-gingerol can significantly reduce the degree of oxi?dative stress and the level of reactive oxygen species caused by cardiomyocyte damage, and has a significant cardiopro?tective effect. ② Anti-inflammatory: inflammation can cause substantial cell damage and organ dysfunction, which is another important cause of myocardial damage. 6-gingerol can reduce the levels of inflammatory factors such as inter?leukin-6, interleukin-1β, and tumor necrosis factor-αin cardiomyocytes, and at the same time inhibit the TLR4/NF-κB sig?naling pathway, an important regulatory pathway of inflammation, showing that it may improve myocardial damage through anti-inflammatory effects. ③ Inhibition of apoptosis: apoptosis is a complex and orderly process in the autono?mous biochemical process of cells, and one of the main mechanisms of myocardial injury. This process can be roughly divided into three pathways: mitochondria, endoplasmic reticulum, and death receptors. Among them, the mitochondrial pathway plays an important role, and Bcl-2 and Bax located upstream of this pathway can regulate the entire process of cell apoptosis by regulating the permeability of the mitochondrial membrane. Studies have found that the preventive application of 6-gingerol can reduce cell damage, reduce the number of apoptotic cells, reduce the activity of Bax and caspase-3, and increase the expression of Bcl-2. Therefore, 6-gingerol pretreatment can reduce the damage of cardio?myocytes, and its mechanism may be related to the inhibition of apoptosis.④Prevent calcium influx:calcium overload is involved in the pathogenesis of myocardial ischemic injury, which may be related to excessive contracture, arrhythmia, and mitochondrial Ca2+accumulation that impairs myocardial function. 6-gingerol inhibits the increase of intracellular Ca2+concentration by inhibiting L-type calcium current, thereby reducing extracellular Ca2+ influx, thereby avoiding calcium overload and playing a cardioprotective effect. In summary, 6-gingerol can effectively treat and improve myocardial isch?emia/reperfusion injury, and it has great development potential in the fields of medicine and health products.

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Article in Chinese | WPRIM | ID: wpr-909604

ABSTRACT

OBJECTIVE To predict the potential targets of hyperoside (Hyp) on improving ischemia/reperfusion injury by network pharmacology, and explore its possible mechanism combined with related literature. METHODS The action targets of Hyp and ischemia/reperfusion injury were obtained by TCMSP, Swiss Target Prediction, Pharm Mapper, Simi?larity ensemble approach, Online Mendelian Inheritance in Man, DisGENT and database. The common targets of drugs and diseases were screened by Omishare and STRING database respectively, and the protein-protein interaction (PPI) network map was constructed. Then the interaction network between Hyp and disease targets was constructed by Cyto?scape software and topological cross-linking analysis was carried out. Then the interaction network between Hyp and disease targets was constructed and cross-linked analysis was carried out by using Cytoscape software. The gene ontol?ogy (GO) of the core target was analyzed by David database, and then the related pathways of the core target were enriched by KEGG database. RESULTS A total of 54 GO enrichment processes were obtained by GO enrichment anal?ysis of 44 common genes, including 38 biological processes (BP), 15 cell composition (CC) processes, and 1 molecular functional (MF) process. 43 items were obtained by signal pathway enrichment analysis in KEGG database. CONCLU?SION It is suggested that the mechanism of Hyp may be related to PI3K-Akt, RAP1, RAS, VEGF and other signal trans?duction pathways. The above results laid a theoretical foundation for the study of the mechanism and clinical application of the treatment of ischemia/reperfusion injury.

18.
Article in Chinese | WPRIM | ID: wpr-909603

ABSTRACT

OBJECTIVE To explore the effect of total flavonoids of Rhododendra simsii (TFR) on improving cerebral ischemia/reperfusion injury (CIRI) and its relationship with STIM/Orai-regulated operational Ca2+influx (SOCE) pathway. METHODS Oxygen-glucose deprivation/reoxygenation (OGD/R) PC12 cells were used to simulate CIRI in vitro, and the intracellular Ca2+ concentration and apoptosis rate of PC12 cells were detected by laser confocal microscope and flow cytometry, respectively. The regulation of STIM/Orai on SOCE was analyzed by STIM/Orai gene silencing and STIM/Orai gene overexpression. The CIRI model was established by MCAO in SD rats. The activities of inflammatory cyto?kines IL-1, IL-6 and TNF-αin serum were detected by ELISA. The pathological changes of ischemic brain tissue and the infarction of rat brain tissue were detected by HE staining and TTC staining. The protein and mRNA expression levels of STIM1, STIM2, Orai1, caspase-3 and PKB in brain tissue were detected by Western blotting and RT-qPCR, respectively. RESULTS The results of in vitro experiment showed that the fluorescence intensity of Ca2+ and apoptosis rate in PC12 cells treated with TFR were significantly lower than those in OGD/R group, and this trend was enhanced by SOCE antagonist 2-APB. STIM1/STIM2/Orai1 gene silencing significantly reduced apoptosis and Ca2+overload in OGD/R model, while TFR combined with overexpression of STIM1/STIM2/Orai1 aggravated apoptosis and Ca2+overload. In the in vivo experiment, TFR significantly reduced the brain histopathological damage, infarction of brain tissue, the contents of IL-1, IL-6 and TNF-α in the serum in MCAO rats and down-regulated the expression of STIM1, STIM2, Orai1 and caspase-3 protein and mRNA in the brain tissue, and up-regulated the expression of PKB. The above effects were enhanced by the addition of 2-APB. CONCLUSION The above results indicate that TFR may reduce the contents of inflammatory factors and apoptosis, decrease Ca2+ overload and ameliorate brain injury by inhibiting SOCE pathway mediated by STIM and Orai, suggesting that it has a protective effect against subacute CIRI.

19.
Article in Chinese | WPRIM | ID: wpr-909522

ABSTRACT

Objective:To explore the effect and molecular mechanism of capsaicin receptor(TRPV1) on neuronal autophagy and depression-like behavior in mice.Methods:Using the method of random number table, 87 C57 male mice were divided into Sham operation group (Sham group), cerebral ischemia/reperfusion group (I/R group) and capsazepine(CPZ) preconditioning cerebral ischemia/reperfusion group (I/R+ CPZ group), with 28 mice in each group due to 3 incompatible.Mice in the I/R group were subjected to right middle cerebral artery occlusion (MCAO) to establish a cerebral ischemia-reperfusion model.Mice in the I/R+ CPZ group were injected with CPZ in the lateral ventricle prior to moulding.Mice in the Sham group had only wire plugs inserted and no arterial embolization was performed.The mNSS score was used to evaluate the degree of neurological deficits.The depression-like behaviour of mice was detected by the tail suspension test and forced swimming test.The infarct volume was observed by TTC staining.The pathological changes in the amygdala were observed by HE staining, and the expression of Beclin-1, LC3, p62 and p-PI3K, p-AKT and p-mTOR proteins were detected by Western blot.Statistical analysis was performed using SPSS 23.0 software.The t-test was used for comparison between two groups and one-way ANOVA was used for comparison of multiple group. Results:The neurological deficit score in I/R+ CPZ group (9.77±2.32) was significantly lower than that in I/R group (12.85±2.73) ( t=3.10, P<0.01). Compared with I/R group, the tail suspension immobility time of I/R+ CPZ Group ((93.28±50.69)s, (143.80±35.61) s; t=2.94, P<0.01) and the forced swimming immobility time ((139.50±13.33)s, (175.30±19.78)s; t=2.94, P<0.01) were significantly reduced.The results of TTC staining showed that the cerebral infarct volume in I/R+ CPZ group was significantly lower than that in I/R group ((19.30±5.19)%, (33.60±3.90)%; t=5.40, P<0.01). HE staining showed that the number of cells in the amygdala region of mice in the I/R+ CPZ group increased compared with that in the I/R group, with tighter arrangement and reduced deep staining of nuclear fixation.Western blot showed that compared with I/R group, the expression levels of autophagy related proteins Beclin-1( t=2.94, P<0.05) and LC3 ( t=3.16, P<0.05) in amygdala of I/R+ CPZ group were down-regulated, while the expression levels of p62( t=3.60, P<0.05), p-PI3K ( t=7.79, P<0.01), p-AKT ( t=4.15, P<0.01) and p-mTOR ( t=6.15, P<0.01) were up-regulated. Conclusion:Cerebral ischemia/reperfusion activates neuronal autophagy, and CPZ may regulate the PI3K-AKT-mTOR pathway, thus inhibits excessive activation of autophagy, thereby acting as a neuroprotective agent and improving post-stroke depression-like behaviour.

20.
Chinese Critical Care Medicine ; (12): 1099-1104, 2021.
Article in Chinese | WPRIM | ID: wpr-909460

ABSTRACT

Objective:To explore the protective effects of bradykinin postconditioning on cardiopulmonary resuscitation (CPR) rats, and to assess the underlying mechanisms.Methods:Forty-eight adult male Sprague-Dawley (SD) rats were randomly divided into four groups according to random number table: Sham operation group, cardiac arrest (CA) group, bradykinin treatment (BK) group, and AMP-activated protein kinase (AMPK) inhibitor Compound C+ bradykinin treatment (CP+BK) group, finally, 8 rats in each group were taken for follow-up experiment. CA was induced by asphyxia. Rats in the Sham group received arteriovenous catheterization, endotracheal intubation, and mechanical ventilation, without CA. Compound C (250 μg/kg) was intraperitoneally injected in CP+BK group 30 minutes before CA, and the same volume of dimethyl sulfoxide (DMSO) was given in the remaining groups. Bradykinin (150 μg/kg) was intraperitoneally injected in BK group and CP+BK group 48 hours after restoration of spontaneous circulation (ROSC), and same volume of saline was given in the remaining groups. The neural function of rats in each group was evaluated with neurological deficit score (NDS) 72 hours after ROSC. Microtubule-associated protein light chain 3 (LC3) and p62 expressions were detected by immunohistochemistry, autophagosomes were observed by transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method (TUNEL) assay was used to assess apoptosis.Results:Compared with the Sham group, the NDS was decreased (60.75±5.80 vs. 80.00±0.00, P < 0.01), the expression levels of LC3 and p62 elevated [LC3 ( A value): 1.04±0.64 vs. 0.40±0.14, p62 ( A value): 2.75±0.57 vs. 0.36±0.12, both P < 0.05], the number of autophagosomes and apoptotic cells increased in the CA group [(39.00±8.00)% vs. (3.87±1.90)%, P < 0.05]. Compared with the CA group, the NDS (67.75±6.32 vs. 60.75±5.80, P < 0.05), the expression of LC3 ( A value: 1.60±0.34 vs. 1.04±0.64, P < 0.05), and the number of autophagosomes increased in the BK group, while the expression of p62 and the rate of apoptotic cells reduced [p62 ( A value): 1.51±0.32 vs. 2.75±0.57, apoptotic cells rate: (23.03±1.91)% vs. (39.00±8.00)%, both P < 0.05]. Compared with the BK group, the NDS (59.00±8.19 vs. 67.75±6.32, P < 0.05), the expression of LC3 ( A value: 0.62±0.41 vs. 1.60±0.34, P < 0.05) and the number of autophagosomes declined in the CP+BK group, while the expression of p62 and the rate of apoptotic cells elevated [p62 ( A value): 3.50±0.47 vs. 1.51±0.32, apoptotic cells rate: (44.53±10.15)% vs. (23.03±1.91)%, both P < 0.05]. Conclusion:Bradykinin postconditioning played a neuroprotective role in CPR rats by activating autophagy and reducing apoptosis.

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