Protective effects of caspase-9 and poly(ADP-ribose) polymerase inhibitors on ischemia-reperfusion-induced myocardial injury

2009 ◽  
Vol 32 (7) ◽  
pp. 1037-1043 ◽  
Author(s):  
Rupinder K. Sodhi ◽  
Manjeet Singh ◽  
Nirmal Singh ◽  
Amteshwar S. Jaggi
Keyword(s):  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Caspase 9 ◽  
Polymerase Inhibitors

Zingerone Alleviates Myocardial Ischemia/Reperfusion Injury

2021 ◽  
Vol 19 (4) ◽  
pp. 543-549
Author(s):  
Fanglin Luo ◽  
Shunxiang Luo ◽  
Yanqing Wu
Keyword(s):  
Myocardial Infarction ◽  
Proinflammatory Cytokine ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Cytokine Release ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Using a rat model, we have explored the underlying mechanism of ischemia/reperfusion (I/R)-mediated myocardial infarction and assessed the protective potential of zingerone. The results show that zingerone exhibits not only the myocardial protective effect, but also antioxidative and anti-inflammatory effects by suppression of markers of oxidation and proinflammatory cytokine release. Zingerone promotes protective effects against I/R-induced myocardial infarction by regulating Nrf2/HO-1 and NF-κB signaling pathways. These findings provide novel insights into the effects of zingerone on the cardioprotective mechanism of myocardial injury after I/R and may open new avenues for myocardial infarction treatment.

The Protective Effects of Ligustrazine on Ischemia-Reperfusion and DPPH Free Radical-Induced Myocardial Injury in Isolated Rat Hearts

Planta Medica ◽  
2004 ◽  
Vol 70 (9) ◽  
pp. 818-822 ◽  
Author(s):  
Yuan Zhou ◽  
Chang-Ping Hu ◽  
Pan-Yue Deng ◽  
Han-Wu Deng ◽  
Yuan-Jian Li
Keyword(s):  
Free Radical ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Rat Hearts ◽  
Isolated Rat

Oxytocin exerts protective effects on in vitro myocardial injury induced by ischemia and reperfusionThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 137-142 ◽  
Author(s):  
Maria Ondrejcakova ◽  
Tatiana Ravingerova ◽  
Jan Bakos ◽  
Dezider Pancza ◽  
Daniela Jezova
Keyword(s):  
Infarct Size ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Control Group ◽  
Protective Effects ◽  
Chronotropic Effect ◽  
Negative Chronotropic Effect

Among the cardiovascular pathologies, ischemic heart disease is a serious medical problem that can result in cardiac injury and (or) heart failure. The aim of the present study was to test the hypothesis that neuropeptide oxytocin induces cardioprotective effects on ischemia–reperfusion-induced myocardial damage. The functional parameters of isolated Langendorff-perfused rat hearts were recorded before and after global 25 min ischemia and subsequent reperfusion. The infarct size was determined by a computerized planimetric method. The results showed that oxytocin produced negative chronotropic effect even at low concentrations (90–125 nmol/L). Perfusion with oxytocin before ischemia resulted in significant reduction of the infarct size (p < 0.01), which was about 66% smaller than that in the control group. To evaluate the functional mechanisms involved, further experiments were performed under conditions of constant heart rate. The lower dose of oxytocin (90 nmol/L), which was ineffective in spontaneously beating hearts, induced a significant decrease of contractility. Elimination of the negative chronotropic effect of oxytocin prevented its cardioprotective action. In conclusion, our results demonstrated an attenuation of the infarct size in oxytocin-treated hearts, indicating a cardioprotective effect of oxytocin. The data suggest that the negative chronotropic action of oxytocin participates in its protective effects on ischemia–reperfusion-induced myocardial injury.

scholarly journals The protective effects of phosphodiesterase-5 inhibitor, sildenafil on post-resuscitation cardiac dysfunction of cardiac arrest: by regulating the miR-155-5p and miR-145-5p

2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Yong He ◽  
Guoxing Wang ◽  
Chuang Li ◽  
Yuxing Wang ◽  
Qian Zhang
Keyword(s):  
Survival Rate ◽  
Myocardial Injury ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Oxygen Metabolism ◽  
Spontaneous Circulation ◽  
Sham Operation ◽  
Protective Effects ◽  
Sham Operation Group

Abstract Background MiRNA-155 and miRNA-145 have been demonstrated to function as a key regulator in the development of the cardiovascular system. Recent experimental and clinical studies have indicated the cardioprotective role of sildenafil during ischemia/reperfusion (I/R) injury. This study was designed to investigate if administration of sildenafil will attenuate post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Methods Thirty-two male pigs (weighing 30 ± 2 kg) were randomly divided into 4 groups, sildenafil group (n = 8), sildenafil +NG-nitro-l-arginine methyl ester (L-NAME) (20 mg/kg L) group (n = 8), saline (SA group, n = 8); and sham operation group (sham group, n = 8). Eight minutes of untreated VF was followed by defibrillation in anesthetized, closed-chest pigs. Hemodynamic status and blood samples were obtained at 0 min, 0.5, 1, 2, 4 and 6 h after return of spontaneous circulation (ROSC), and the hearts were removed and analyzed under electron microscopy, quantitative real-time polymerase chain reaction and ultra structural analysis were performed to evaluate myocardial injury. Results Compared with the sildenafil + L-NAME and saline groups, the sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, and attenuated myocardial injury; In this study, CA pigs showed evidently increased levels of miR-155-5p and miR-145-5p, while the sildenafil treatment decreased the levels of miR-155-5p and miR-145-5p in CA pigs. In addition, the levels of eNOS was decreased in CA pigs, validating sildenafil attenuating post-resuscitation myocardial dysfunction by regulating miRNA-155 and miR-145 expressions. Conclusions Sildenafil group had better outcomes in terms of hemodynamic and oxygen metabolism parameters as well as 24-h survival rate, inhibited the increases in the miR-155-5p and miR-145-5p levels and attenuated myocardial injury in a porcine model of CA and resuscitation.

Protective effects of sitagliptin on myocardial injury and cardiac function in an ischemia/reperfusion rat model

2013 ◽  
Vol 718 (1-3) ◽  
pp. 105-113 ◽  
Author(s):  
Guanglei Chang ◽  
Peng Zhang ◽  
Lin Ye ◽  
Kai Lu ◽  
Ying Wang ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Rat Model ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects

scholarly journals Alleviation of Hepatic Ischemia Reperfusion Injury by Oleanolic Acid Pretreating via Reducing HMGB1 Release and Inhibiting Apoptosis and Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Wenwen Wang ◽  
Liwei Wu ◽  
Jingjing Li ◽  
Jie Ji ◽  
Kan Chen ◽  
...  
Keyword(s):  
Oleanolic Acid ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
Protective Effects ◽  
Caspase 9 ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Underlying Mechanisms ◽  
Necrosis Factor

Hepatic ischemia reperfusion (IR) injury (IRI) occurs during liver transplantation, hepatectomy, and hemorrhagic shock. Oleanolic acid (OA) is a natural compound with antioxidant and anti-inflammatory activity that has been used to treat liver disorders in clinical practice for several years. Here, we investigated the effects and underlying mechanisms of OA in hepatic IRI. A 60-minute partial (70%) hepatic, warm, ischemic reperfusion model was established in BALB/c mice, and two doses (30 and 60 mg/kg) of OA were administered intragastrically for 7 consecutive days prior to hepatic IR. Orbital blood and liver specimens were collected at 2, 8, and 24 h after IR. The results showed that OA preconditioning significantly alleviated hepatic injury, as evidenced by decreased alanine aminotransferase and aspartate aminotransferase levels; improved histology, inhibition of JNK phosphorylation, and high mobility group box 1 (HMGB1); and tumor necrosis factor-α downregulation in hepatic IR mice. OA upregulated Bcl-2 and downregulated caspase-3, caspase-9, Bax, Beclin 1, and LC3, which play crucial roles in the regulation of apoptosis and autophagy. These findings highlighted the protective effects of OA against hepatic IRI mediated by the inhibition of apoptosis and autophagy and the release of HMGB1, which acted as a late inflammatory mediator in hepatic IRI.

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