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对羟基肉桂酸通过抑制氧化应激减轻异丙肾上腺素诱导的心肌梗死大鼠的细胞凋亡。

p-Coumaric acid attenuates apoptosis in isoproterenol-induced myocardial infarcted rats by inhibiting oxidative stress.

机构信息

Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar - 608002, Tamil Nadu, India.

出版信息

Int J Cardiol. 2013 Oct 9;168(4):3259-66. doi: 10.1016/j.ijcard.2013.04.138. Epub 2013 May 16.

Abstract

BACKGROUND

Cardiac apoptosis plays an important role in the pathology of myocardial infarction. The protective effects of p-coumaric acid on cardiac apoptosis were evaluated in isoproterenol induced myocardial infarcted rats.

METHODS

Rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days. After pretreatment, isoproterenol (100 mg/kg body weight) was injected subcutaneously into rats at an interval of 24 h for 2 days to induce myocardial infarction. Cardiac diagnostic markers, heart lipid peroxidation, antioxidant system, histopathological changes of the heart and apoptosis were evaluated in isoproterenol induced myocardial infarcted rats.

RESULTS

Isoproterenol induced myocardial infarcted rats showed a significant increase in the levels of serum cardiac diagnostic markers, heart lipid peroxidation products and a significant decrease in the activities/levels of heart antioxidants. Histopathological findings of myocardial infarcted rats revealed marked necrosis and edema. Reverse Transcription Polymerase Chain Reaction study revealed an increase in the myocardial expression of Bax, caspase-8, caspase-9 and Fas genes and a decrease in the myocardial expression of Bcl-2 and Bcl-xL genes. p-Coumaric acid pretreatment showed protective effects on apoptosis by inhibiting oxidative stress. p-Coumaric acid pretreated isoproterenol induced myocardial infarcted heart also confirmed these findings. The possible mechanisms for the protective effects of p-coumaric acid could be attributed to antilipid peroxidative, antioxidant and antiapoptotic properties.

CONCLUSION

Thus, p-coumaric acid protected the myocardial infarcted rat's heart against apoptosis by inhibiting oxidative stress.

摘要

背景

心脏细胞凋亡在心肌梗死的病理学中起着重要作用。本研究旨在评估对羟基肉桂酸(p- 香豆酸)对异丙肾上腺素诱导的心肌梗死大鼠心脏细胞凋亡的保护作用。

方法

大鼠预先每天用对羟基肉桂酸(8mg/kg 体重)处理 7 天。预处理后,异丙肾上腺素(100mg/kg 体重)每隔 24 小时皮下注射到大鼠体内,连续 2 天以诱导心肌梗死。评估异丙肾上腺素诱导的心肌梗死大鼠的心脏诊断标志物、心脏脂质过氧化、抗氧化系统、心脏组织病理学变化和细胞凋亡。

结果

异丙肾上腺素诱导的心肌梗死大鼠血清心脏诊断标志物水平、心脏脂质过氧化产物显著增加,心脏抗氧化剂的活性/水平显著降低。心肌梗死大鼠的组织病理学检查显示明显的坏死和水肿。逆转录聚合酶链反应研究显示,Bax、caspase-8、caspase-9 和 Fas 基因在心肌中的表达增加,Bcl-2 和 Bcl-xL 基因在心肌中的表达减少。对羟基肉桂酸预处理通过抑制氧化应激显示出对细胞凋亡的保护作用。对羟基肉桂酸预处理的异丙肾上腺素诱导的心肌梗死大鼠心脏也证实了这些发现。对羟基肉桂酸的保护作用的可能机制可归因于抗脂质过氧化、抗氧化和抗凋亡特性。

结论

因此,对羟基肉桂酸通过抑制氧化应激来保护心肌梗死大鼠的心脏免受细胞凋亡。

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