Chinese medicinal formula Guanxin Shutong capsule protects the heart against oxidative stress and apoptosis induced by ischemic myocardial injury in rats.

Chinese medicinal formula Guanxin Shutong capsule protects the heart against oxidative stress and apoptosis induced by ischemic myocardial injury in rats.
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DOI:
10.3892/etm.2014.1540
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发表时间:
2014-04
影响因子:
2.7
通讯作者:
Zhang Y
Zhang Y
中科院分区:
医学4区
文献类型:
--
作者:
Cao Y;He X;Lui F;Huang Z;Zhang Y

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冠心舒通胶囊(GXSTC)是一种中药配方,在我国临床用于治疗胸痛、抑郁、心悸和心血管疾病已有近10年的历史。本研究的目的是探讨 GXSTC 在心肌缺血 (MI) 大鼠心脏中对抗氧化应激和细胞凋亡的保护机制。通过生化分析测定梗塞面积和标记酶的水平,包括血清肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)和谷氨酸草酰乙酸转氨酶(GOT),以及心脏中一氧化氮(NO)和一氧化氮合成酶(NOS)的水平。还测定了抗氧化剂超氧化物歧化酶 (SOD)、过氧化氢酶 (CATA) 和谷胱甘肽 (GSH) 以及氧化应激标记物丙二醛 (MDA) 的水平。缺血 6 周后,评估心肌细胞凋亡以及 NADPH 氧化酶的蛋白质和 mRNA 表达。使用蛋白质印迹分析通过 p47phox 和 gp91phox 的蛋白表达以及使用逆转录聚合酶链式反应通过 p22phox、p47phox、p67phox 和 gp91phox 的 mRNA 表达来测量心肌 NADPH 氧化酶活性。结果显示,与媒介物治疗的MI模型大鼠相比,每日口服GXSTC的大鼠可减少梗死面积、心肌细胞凋亡、血清MDA、LDH、CK-MB和GOT以及心脏GOT的水平,并增加总SOD、CATA、NOS的活性以及NO和GSH的水平。给予 GXSTC 6 周还降低了 NADPH 氧化酶亚基 p47phox 和 gp91phox 蛋白的 mRNA 表达,以及 Bax 和 caspase-3 蛋白的表达。相比之下,Bcl-2蛋白表达增加。总之,结果表明 GXSTC 通过抗氧化和抗凋亡作用减轻心肌损伤。
Guanxin Shutong capsule (GXSTC) is a Chinese medicinal formula that has been used clinically for the treatment of chest pain, depression, palpitation and cardiovascular diseases in China for almost 10 years. The aim of the present study was to investigate the protective mechanisms against oxidative stress and apoptosis that GXSTC exhibits in the hearts of rats with myocardial ischemia (MI). Infarct size and the levels of marker enzymes, including serum creatine kinase-isoenzyme (CK-MB), lactate dehydrogenase (LDH) and glutamate oxaloacetic transaminase (GOT), as well as the levels of nitric oxide (NO) and NO synthase (NOS) in the heart were measured by biochemical analysis assays. Levels of the antioxidants superoxide dismutase (SOD), catalase (CATA), and glutathione (GSH), and the oxidative stress marker malondialdehyde (MDA), were also determined. Following a 6-week period of ischemia, myocardial apoptosis, as well as the protein and mRNA expression of NADPH oxidase, was evaluated. Myocardial NADPH oxidase activity was measured by protein expression of p47phox and gp91phox using western blot analysis and mRNA expression of p22phox, p47phox, p67phox and gp91phox using reverse transcription polymerase chain reaction. The results showed that daily oral treatment of the rats with GXSTC reduced infarct size, myocardial apoptosis, the levels of serum MDA, LDH, CK-MB and GOT and heart GOT, and increased the activities of total SOD, CATA, NOS and the levels of NO and GSH compared with those in vehicle-treated MI model rats. Administration of GXSTC for 6 weeks also reduced the mRNA expression of the NADPH oxidase subunits p47phox and gp91phox protein, as well as the expression of Bax and caspase-3 proteins. By contrast, Bcl-2 protein expression increased. In conclusion, the results demonstrate that GXSTC attenuates myocardial injury via antioxidative and antiapoptotic effects.
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