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IGF-1通过激活大鼠PI3K/Akt信号通路对心肌缺血/再灌注损伤的心脏保护作用

Cardioprotective effect of IGF-1 against myocardial ischemia/reperfusion injury through activation of PI3K/Akt pathway in rats .

作者信息

Liao Yaojun, Li Hong, Pi Yanna, Li Zijia, Jin Sanqing

机构信息

Department of Anaesthesia, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong Province, China.

出版信息

J Int Med Res. 2019 Aug;47(8):3886-3897. doi: 10.1177/0300060519857839. Epub 2019 Jul 25.

DOI:10.1177/0300060519857839
PMID:31342837
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6726826/
Abstract

OBJECTIVE

It remains unknown whether insulin-like growth factor-1 (IGF-1) can attenuate myocardial ischemia/reperfusion (I/R) injury by activating the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway. This study investigated the possible interaction of IGF-1 with the PI3K/Akt pathway in cardioprotection against myocardial I/R injury in rats.

METHODS

We established a myocardial I/R model in rats through left anterior descending artery ligation for 40 minutes followed by 6 hours reperfusion. The PI3K/Akt inhibitor, LY294002 (0.3 mg/kg), was injected through the caudal vein 30 minutes before myocardial ischemia, and IGF-1 (1 µg/kg or 5 µg/kg) was injected through the caudal vein 10 minutes before myocardial ischemia.

RESULTS

IGF-1 treatment decreased myocardial infarct size; myocardial cell apoptosis; and serum lactate dehydrogenase, creatine kinase MB, and cardiac troponin I levels in rats with myocardial I/R . Moreover, IGF-1 treatment led to significant increases in expression levels of p-Akt (Ser473) and B cell lymphoma 2, while reducing expression levels of caspase-9 mRNA and cleaved caspase-9 protein in rats with myocardial I/R. However, pretreatment with LY294002 significantly reduced the cardioprotective effects of IGF-1.

CONCLUSION

Treatment with IGF-1 may confer cardiac protection against myocardial I/R injury via the PI3K/Akt pathway in rats.

摘要

目的

胰岛素样生长因子-1（IGF-1）是否能通过激活磷酸肌醇3激酶/蛋白激酶B（PI3K/Akt）信号通路减轻心肌缺血/再灌注（I/R）损伤尚不清楚。本研究探讨IGF-1与PI3K/Akt信号通路在大鼠心肌I/R损伤心脏保护中的可能相互作用。

方法

通过结扎大鼠左前降支40分钟，然后再灌注6小时建立心肌I/R模型。在心肌缺血前30分钟经尾静脉注射PI3K/Akt抑制剂LY294002（0.3mg/kg），在心肌缺血前10分钟经尾静脉注射IGF-1（1μg/kg或5μg/kg）。

结果

IGF-1治疗可减小心肌I/R大鼠的心肌梗死面积、心肌细胞凋亡，降低血清乳酸脱氢酶、肌酸激酶同工酶MB和心肌肌钙蛋白I水平。此外，IGF-1治疗可使心肌I/R大鼠的p-Akt（Ser473）和B细胞淋巴瘤-2表达水平显著升高，同时降低caspase-9 mRNA和裂解的caspase-9蛋白表达水平。然而，LY294002预处理显著降低了IGF-1的心脏保护作用。

结论

IGF-1治疗可能通过PI3K/Akt信号通路对大鼠心肌I/R损伤起到心脏保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/becb9ce699e3/10.1177_0300060519857839-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/9d2143c1cda6/10.1177_0300060519857839-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/c43078b67c82/10.1177_0300060519857839-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/e480ea133213/10.1177_0300060519857839-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/becb9ce699e3/10.1177_0300060519857839-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/9d2143c1cda6/10.1177_0300060519857839-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/c43078b67c82/10.1177_0300060519857839-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/e480ea133213/10.1177_0300060519857839-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8019/6726826/becb9ce699e3/10.1177_0300060519857839-fig4.jpg

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