scholarly journals Huang Qi Tong Bi Decoction Attenuates Myocardial Ischemia-Reperfusion Injury via HMGB1/TLR/NF-κB Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Kun Liu ◽  
Manman Li ◽  
Xiumei Ren ◽  
Qing-sheng You ◽  
Fei Wang ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Reperfusion Injury ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
St Segment ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

The aim of this study was to study the protective effect of Huang Qi Tong Bi Decoction (HQTBT) on the heart of rats. Ischemia-reperfusion injury was established by coronary artery ligation. Proinflammatory cytokines were decreased by XFZY in coronary artery ligated rats. ST segment was also restored with the treatment of HQTBT. Triphenyltetrazole chloride (TTC) staining and pathological analysis showed that HQTBT reduced myocardial injury. Besides, the expressions of HMGB1/TLR/NF-κB pathway in rats were significantly decreased by HQTBT. This study shows that HQTBT inhibited inflammatory reaction on myocardial injury in rats.

scholarly journals Mangiferin Attenuates Myocardial Ischemia-Reperfusion Injury via MAPK/Nrf-2/HO-1/NF-κB In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Kun Liu ◽  
Fei Wang ◽  
Shuo Wang ◽  
Wei-Nan Li ◽  
Qing Ye
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
H9c2 Cells ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

The aim of this study was to investigate the cardioprotective effect of mangiferin (MAF) in vitro and in vivo. Oxidative stress and inflammatory injury were detected in coronary artery ligation in rats and also in hypoxia-reoxygenation- (H/R-) induced H9c2 cells. MAF inhibited myocardial oxidative stress and proinflammatory cytokines in rats with coronary artery occlusion. The ST segment of MAF treatment groups also resumed. Triphenyltetrazolium chloride (TTC) staining and pathological analysis showed that MAF could significantly reduce myocardial injury. In vitro data showed that MAF could improve hypoxia/reoxygenation- (H/R-) induced H9c2 cell activity. In addition, MAF could significantly reduce oxidative stress and inflammatory pathway protein expression in H/R-induced H9c2 cells. This study has clarified the protective effects of MAF on myocardial injury and also confirmed that oxidative stress and inflammation were involved in the myocardial ischemia-reperfusion injury (I/R) model.

scholarly journals NARINGIN ATTENUATES OXIDATIVE STRESS AND PROTECT AGAINST MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN DIABETIC RAT

2019 ◽  
pp. 230-234
Author(s):  
NEELAM KUMARI ◽  
AJAY SINGH KUSHWAH
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
The Body ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Coronary Artery Ligation ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective: The relative risk of coronary heart disease in diabetic patients is more than in non-diabetic population. The present study was undertaken to explore the cardioprotective effect of Naringin on ischemia-reperfusion injury in the diabetic model of rat. Methods: Adult Wistar rats (either sex) divided into six groups. Diabetes was induced by 5 weeks combine exposure to a high-fat diet with a low dose of streptozotocin (30 mg/kg i.p.), administered on the 1st day of starting of the 5th week. Naringin treatment 25 mg/kg and 50 mg/kg was given simultaneously for 5 weeks. On the 36th day, the study animals were subjected to induction myocardial ischemia-reperfusion injury induced by the ligation of the left anterior descending coronary artery ligation in anesthetizing rat. Serum glucose level and cholesterol level measured before performing of ischemic reperfusion. After reperfusion injury, the animals were sacrificed and estimate change in the heart in the course of biochemical alterations, in creatine kinase-muscle/ brain (CK-MB) and lactate dehydrogenase, lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD) and infarct size in the heart. Results and Conclusion: Naringin treatment significantly reduced the body weight, blood glucose, cholesterol, cardiac injury biomarkers, and LPO level and increased in antioxidant (GSH and SOD) level and also significantly increased in mean arterial pressure heart rate, reduced the myocardial infarction size. The present study concludes that Naringin 50 mg/kg being more prominent action to reduce the cardiotoxicity risk in ischemia-reperfusion injury state and increases myocardial susceptibility through having more prominent antioxidant potential properties.

scholarly journals Effectiveness ofPanax ginsengon Acute Myocardial Ischemia Reperfusion Injury Was Abolished by Flutamide via Endogenous Testosterone-Mediated Akt Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Luo Pei ◽  
Hou Shaozhen ◽  
Dong Gengting ◽  
Chen Tingbo ◽  
Liu Liang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Panax Ginseng ◽  
Testosterone Level ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Artery Ligation ◽  
Protective Mechanisms ◽  
Artery Ligation ◽  
Measured Time ◽  
Myocardial Ischemia Reperfusion

Mechanisms forPanax ginseng’s cardioprotective effect against ischemia reperfusion injury involve the estrogen-mediated pathway, but little is known about the role of androgen. A standardizedPanax ginsengextract (RSE) was orally given with or without flutamide in a left anterior descending coronary artery ligation rat model. Infarct size, CK and LDH activities were measured. Time-related changes of NO, PI3K/Akt/eNOS signaling, and testosterone concentration were also investigated. RSE (80 mg/kg) significantly inhibited myocardial infarction and CK and LDH activities, while coadministration of flutamide abolished this effect of RSE. NO was increased by RSE and reached a peak after 15 min of ischemia; however, flutamide cotreatment suppressed this elevation. Western blot analysis showed that RSE significantly reversed the decreases of expression and activation of PI3K, Akt, and eNOS evoked by ischemia, whereas flutamide attenuated the effects of these protective mechanisms induced by RSE. RSE completely reversed the dropping of endogenous testosterone level induced by I/R injury. Flutamide plus RSE treatment not only abolished RSE’s effect but also produced a dramatic change on endogenous testosterone level after pretreatment and ischemia. Our results for the first time indicate that blocking androgen receptor abolishes the ability ofPanax ginsengto protect the heart from myocardial I/R injury.

scholarly journals Autophagic Flux Impairment Exacerbates Myocardial Ischemia-Reperfusion Injury in Experimental Diabetes Through Atg5/LAMP2 Cleavage by Calpains

2020 ◽  
Author(s):  
Lichun Guan ◽  
Ziqin Yu ◽  
Zhimei Che ◽  
Hang Zhang ◽  
Yong Yu ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Heart ◽  
Autophagic Flux ◽  
Coronary Artery Ligation ◽  
Negative Effects ◽  
Artery Ligation ◽  
R Process ◽  
Myocardial Ischemia Reperfusion

Abstract Background: is a chronic metabolic disease characterized by hyperglycemia, which has negative effects on cardiac revascularization in patients with coronary artery disease (CAD). Methods: This study focused on the role of autophagic flux in regulating susceptibility of STZ-induced diabetic heart to ischemia-reperfusion (I/R) injury. We established STZ-induced diabetes mice and perform I/R process by coronary artery ligation, and neonatal mice cardiomyocytes culture subjected to high glucose and hypoxia/reoxygenation(H/R). Results: Diabetic heart was more sensitive to I/R injury. Autophagic flux, represented by TEM, relative LC3Ⅱ changes under CQ intervention and P62 expression, was impaired in diabetic hearts and deteriorated during subsequent I/R. Calpains were activated in diabetic I/R heart, and the inhibition of calpains partially rescued autophagic flux, cardiac function, and cell death. The expression of autophagic flux related proteins Atg5 and LAMP2 decreased significantly in diabetic I/R heart. Further studies suggested that calpain could cleave Atg5 and LAMP2, and generate cleaved fragments, which might be reversed by calpain inhibition. Inhibition of calpain，or in company with overexpression of Atg5 and LAMP2 , could reduce myocardial injury in diabetic heart subject to I/R. But overexpression of Atg5 alone could worsen the I/R injury. Conclusion: In conclusion, calpain-mediated cleavage of Atg5 and LAMP2 accounts for the impaired autophagic flux which increases the susceptibility to myocardial I/R injury in experimental diabetic mice.

scholarly journals Mechanisms of ranolazine pretreatment in preventing ventricular tachyarrhythmias in diabetic db/db mice with acute regional ischemia–reperfusion injury

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chung-Chuan Chou ◽  
Hui-Ling Lee ◽  
Gwo-Jyh Chang ◽  
Hung-Ta Wo ◽  
Tzung-Hai Yen ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Artery Ligation ◽  
Ventricular Tachyarrhythmias ◽  
Artery Ligation ◽  
Electrophysiological Studies ◽  
Myocardial Ischemia Reperfusion

AbstractStudies have demonstrated that diabetic (db/db) mice have increased susceptibility to myocardial ischemia–reperfusion (IR) injury and ventricular tachyarrhythmias (VA). We aimed to investigate the antiarrhythmic and molecular mechanisms of ranolazine in db/db mouse hearts with acute IR injury. Ranolazine was administered for 1 week before coronary artery ligation. Diabetic db/db and control db/+ mice were divided into ranolazine-given and -nongiven groups. IR model was created by 15-min left coronary artery ligation and 10-min reperfusion. In vivo electrophysiological studies showed that the severity of VA inducibility was higher in db/db mice than control (db/ +) mice. Ranolazine suppressed the VA inducibility and severity. Optical mapping studies in Langendorff-perfused hearts showed that ranolazine significantly shortened action potential duration, Cai transient duration, Cai decay time, ameliorated conduction inhomogeneity, and suppressed arrhythmogenic alternans induction. Western blotting studies showed that the expression of pThr17-phospholamban, calsequestrin 2 and voltage-gated sodium channel in the IR zone was significantly downregulated in db/db mice, which was ameliorated with ranolazine pretreatment and might play a role in the anti-arrhythmic actions of ranolazine in db/db mouse hearts with IR injury.

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