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人参皂苷Rh3通过抑制p38丝裂原活化蛋白激酶/半胱天冬酶-3信号通路诱导的细胞凋亡对大鼠心肌缺血再灌注损伤模型的保护作用。

Protective action of the ginsenoside Rh3 in a rat myocardial ischemia-reperfusion injury model by inhibition of apoptosis induced via p38 mitogen-activated protein kinase/caspase-3 signaling.

作者信息

Cao Liexiang, Gao Yi, Zhu Jinqiang, Zhang Jinbo, Dong Meiping, Mao Yi

机构信息

Emergency Center, The First People's Hospital of Wenling, Wenling, Zhejiang, China.

Department of Anesthesiology, The First People's Hospital of Wenling, Wenling, Zhejiang, China.

出版信息

J Int Med Res. 2020 Dec;48(12):300060520969090. doi: 10.1177/0300060520969090.

DOI:10.1177/0300060520969090
PMID:33284724
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7724424/
Abstract

OBJECTIVE

To investigate the protective effects of the ginsenoside Rh3 on rats subjected to myocardial ischemia-reperfusion (MIR) via its impact on caspase-3 and the p38 mitogen-activated protein kinase (MAPK) pathway.

METHODS

Fifteen male Sprague-Dawley rats were randomly categorized into the MIR group (MY group, n = 5), sham surgery group (SS group, n = 5), and ginsenoside Rh3 group (GR group, n = 5).

RESULTS

The MY group exhibited the largest myocardial infarctions compared with the GR and SS groups. The GR group exhibited significantly higher cell viability of cardiomyocytes and significantly decreased apoptosis compared with the MY group. Fibrils of infarcted tissue in the GR group were disordered but less swollen, with a more organized fibril orientation than those in the MY group. The GR group showed reduced p-p38 MAPK protein and caspase-3 mRNA expression levels compared with the MY and SS groups.

CONCLUSIONS

Rh3 significantly improved myocardial necrosis and caspase-3 levels in myocardial tissues by suppressing the p38 MAPK pathway, thereby inhibiting caspase-3 involvement in apoptosis. Thus, Rh3 was effective in inhibiting the escalated apoptotic pathway in myocardial infarction and can potentially serve as a useful therapeutic agent to rescue myocardial infarction.

摘要

目的

通过研究人参皂苷Rh3对心肌缺血再灌注(MIR)大鼠体内半胱天冬酶-3(caspase-3)和p38丝裂原活化蛋白激酶(MAPK)信号通路的影响,探讨其对大鼠MIR损伤的保护作用。

方法

将15只雄性Sprague-Dawley大鼠随机分为心肌缺血再灌注组(MY组,n = 5)、假手术组(SS组,n = 5)和人参皂苷Rh3组(GR组,n = 5)。

结果

与GR组和SS组相比,MY组心肌梗死面积最大。与MY组相比,GR组心肌细胞活力显著升高,细胞凋亡显著减少。GR组梗死组织的肌原纤维排列紊乱但肿胀程度较轻,与MY组相比,肌原纤维排列更有序。与MY组和SS组相比,GR组p-p38 MAPK蛋白表达水平及caspase-3 mRNA表达水平降低。

结论

Rh3通过抑制p38 MAPK信号通路,显著改善心肌组织坏死及caspase-3水平,从而抑制caspase-3参与细胞凋亡。因此,Rh3能有效抑制心肌梗死中凋亡途径的激活,有望成为挽救心肌梗死的有效治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/6ce47ab4450e/10.1177_0300060520969090-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/64b17211a7c4/10.1177_0300060520969090-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/778516b84f34/10.1177_0300060520969090-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/cf46bc830588/10.1177_0300060520969090-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/e1d79ce357d4/10.1177_0300060520969090-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/81a6bd7301c2/10.1177_0300060520969090-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/52377b78697a/10.1177_0300060520969090-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/6ce47ab4450e/10.1177_0300060520969090-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/64b17211a7c4/10.1177_0300060520969090-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/778516b84f34/10.1177_0300060520969090-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/cf46bc830588/10.1177_0300060520969090-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/e1d79ce357d4/10.1177_0300060520969090-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/81a6bd7301c2/10.1177_0300060520969090-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/52377b78697a/10.1177_0300060520969090-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/7724424/6ce47ab4450e/10.1177_0300060520969090-fig7.jpg

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