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BNC 通过 ERK1/2 信号通路保护 H9c2 心肌细胞免受 H 2 O 2 诱导的氧化损伤。

BNC Protects H9c2 Cardiomyoblasts from H 2 O 2 -Induced Oxidative Injury through ERK1/2 Signaling Pathway.

机构信息

Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China.

出版信息

Evid Based Complement Alternat Med. 2013;2013:802784. doi: 10.1155/2013/802784. Epub 2013 Oct 10.

Abstract

Buchang naoxintong capsule (BNC) is a traditional Chinese medicine approved for the treatment of cerebrovascular and cardiovascular diseases. However, little is known about the specific protective function or mechanism by which BNC protects against myocardial injury. This research was designed to investigate the cardioprotective effects of BNC in vitro model of hydrogen peroxide (H2O2)-induced H9c2 rat cardiomyoblasts. BNC intestinal absorption liquid was used in this study instead of drug-containing serum or extracting solution. Our study revealed that BNC preconditioning enhanced antioxidant function by increasing the activities of total-antioxygen capacity, total-superoxide dismutase, and catalase and by decreasing the production of reactive oxygen species and malondialdehyde. BNC preconditioning also activated extracellular signal-regulated kinases (ERK1/2) and inhibited apoptosis-related proteins such as poly ADP-ribose polymerase (PARP) and caspase-3. Additionally, preincubation with BNC reduced intracellular Ca(2+) concentration, improved mitochondrial membrane potential, and decreased the apoptosis rate of H9c2 cells in a dose-dependent manner. These data demonstrated that BNC protects H9c2 cardiomyoblasts from H2O2-induced oxidative injury by increasing antioxidant abilities, activating ERK1/2, and blocking Ca(2+)-dependent and mitochondria-mediated apoptosis. Based on our results, the potency of BNC for protecting H9c2 cells from oxidative damage is comparable to that of trimetazidine.

摘要

步长脑心通胶囊(BNC)是一种被批准用于治疗心脑血管疾病的中药。然而,对于 BNC 如何保护心肌免受损伤的具体保护功能或机制知之甚少。本研究旨在研究 BNC 在体外过氧化氢(H2O2)诱导的 H9c2 大鼠心肌细胞损伤模型中的心脏保护作用。本研究使用 BNC 肠吸收液代替含药血清或提取液。我们的研究表明,BNC 预处理通过增加总抗氧化能力、总超氧化物歧化酶和过氧化氢酶的活性,减少活性氧和丙二醛的产生,增强了抗氧化功能。BNC 预处理还激活了细胞外信号调节激酶(ERK1/2),并抑制了多聚 ADP-核糖聚合酶(PARP)和半胱天冬酶-3 等凋亡相关蛋白。此外,BNC 的预孵育以剂量依赖的方式降低了细胞内 Ca(2+)浓度,改善了线粒体膜电位,并降低了 H9c2 细胞的凋亡率。这些数据表明,BNC 通过增加抗氧化能力、激活 ERK1/2 以及阻断 Ca(2+)依赖性和线粒体介导的凋亡,保护 H9c2 心肌细胞免受 H2O2 诱导的氧化损伤。根据我们的结果,BNC 保护 H9c2 细胞免受氧化损伤的效力可与曲美他嗪相媲美。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0141/3810482/4556bb314911/ECAM2013-802784.001.jpg

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