芍药苷
丙二醛
免疫印迹
超氧化物歧化酶
再灌注损伤
p38丝裂原活化蛋白激酶
药理学
心肌梗塞
医学
化学
缺血
内分泌学
内科学
激酶
MAPK/ERK通路
氧化应激
生物化学
色谱法
高效液相色谱法
基因
作者
Fubin Wu,Bin-Hua Ye,Xiandan Wu,Xian Yong Lin,Yanyan Li,Yongning Wu,Linping Tong
出处
期刊:Pharmacology
[Karger Publishers]
日期:2019-10-16
卷期号:105 (5-6): 281-288
被引量:34
摘要
<b><i>Objective:</i></b> To study the myocardial benefit effect and mechanism of paeoniflorin on myocardial ischemia reperfusion injury (MIRI) in rats. <b><i>Methods:</i></b> Hundred SD rats were randomly divided into 5 groups: sham group, model group, Paeoniflorin (15 mg/kg) group, Paeoniflorin (30 mg/kg) group, and Paeoniflorin (60 mg/kg) group. Myocardial ischemia reperfusion model was established in each group except the sham group. The myocardial infarction and morphological changes were measured by the TTC staining and HE staining respectively. Myocardial caspase-3 was detected by immunohistochemistry. In addition, the protein levels of Bcl-2 and Bax and the expression ratio of p-erk, p-jnk, and p-p38 were detected by Western blot. Myocardial superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured by the assay kit. <b><i>Results:</i></b> Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can obviously alleviate myocardial infarction caused by MIRI (<i>p</i> < 0.05). HE staining showed that the myocardial morphology in the treatment group was obviously better than that in the model group. WB and immunohistochemistry showed that Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can significantly increase the reduced protein level of bcl-2 (<i>p</i> < 0.05) and reduce the increased protein level of caspase3, bax p-erk, p-jnk, and p-p38 caused by MIRI (<i>p</i> < 0.05). The activity of SOD was increased and the level of MDA was decreased after Paeoniflorin treatment. <b><i>Conclusion:</i></b> Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to reducing oxidative stress and apoptosis by inhibiting the expression of apoptosis-related signaling pathway.
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