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青藤碱对大鼠心肌缺血/再灌注损伤的心脏保护作用

Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model.

作者信息

Lu Changhong, Guo Xiao, He Xianghui, Chang Yu, Zheng Fa, Xu Chenji, Zhang Shuwen, Zhou Yaqun, Li Junfang

机构信息

Department of Heart Center, Qingdao Fuwai Cardiovascular Hospital, No.201 Nanjing Road, Qingdao City, Shandong Province 266034, China.

Department of Emergency, Qingdao Fuwai Cardiovascular Hospital, No.201 Nanjing Road, Qingdao City, Shandong Province 266034, China.

出版信息

Saudi Pharm J. 2022 Jun;30(6):669-678. doi: 10.1016/j.jsps.2022.04.005. Epub 2022 Apr 21.

Abstract

BACKGROUND

Ischemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.

METHODS

Rat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.

RESULTS

Pre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.

CONCLUSION

Our result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.

摘要

背景

缺血再灌注(I/R)在心血管疾病的发展中起着至关重要的作用。青藤碱(SM)已被证明具有抗氧化、抗癌、抗炎、抗病毒和抗致癌特性。本研究旨在探讨SM对大鼠I/R损伤的心脏保护作用。

方法

将大鼠随机分为正常对照组(NC)、I/R对照组和I/R + SM组(5、10和20 mg/kg)。评估室性心律失常、体重和心脏重量。检测抗氧化剂、炎性细胞因子、炎性介质和纤溶系统指标。

结果

预处理的SM组大鼠在缺血(30和120分钟)期间,室颤、室性早搏(VEB)和室性心动过速的持续时间和发生率降低,心律失常评分受到抑制。SM处理的大鼠抗氧化参数水平显著改变(P < 0.001)。SM处理显著(P < 0.001)降低了肌酸激酶MB(CK-MB)、肌酸激酶(CK)和肌钙蛋白I(Tnl)的水平。SM处理的大鼠显著(P < 0.001)抑制了组织因子(TF)、血栓素B2(TXB2)、纤溶酶原激活物抑制剂1(PAI-1)和血浆纤维蛋白原(Fbg)以及炎性细胞因子和炎性介质。

结论

我们的结果清楚地表明,SM通过改变氧化应激和炎症反应对大鼠I/R损伤发挥抗心律失常作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9257858/3d7ba71401bc/gr1.jpg

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