蛋白激酶B
再灌注损伤
细胞凋亡
氧化应激
医学
PI3K/AKT/mTOR通路
缺血
LY294002型
生物
促炎细胞因子
药理学
化学
信号转导
细胞生物学
心肌保护
磷酸化
炎症
癌症研究
内科学
内分泌学
免疫学
生物化学
作者
Z-Q Lv,Chunzhang Yang,Q-S Xing
出处
期刊:PubMed
日期:2020-04-01
卷期号:24 (7): 4005-4015
被引量:4
标识
DOI:10.26355/eurrev_202004_20870
摘要
Myocardial ischemia reperfusion injury (MIRI) is a common factor in heart-related diseases. The aim of this study was to explore the effect of TRIM59 gene on MIRI and its mechanism.Rats were used to construct MIRI models, and TRIM59 gene was overexpressed in myocardium by Entranster technique to detect the effects of TRIM59 on myocardial oxidative stress, myocardial injury, and ATPase. In addition, rat myocardial H9c2 cells were cultured, and a hypoxia-reoxygenation model of H9c2 cells was constructed to detect the effect of TRIM59 overexpression on the inflammation and apoptosis of H9c2 cells. Finally, the PI3K/Akt signaling pathway inhibitor LY294002 was used to study the effect of TRIM59 on the PI3K/Akt signaling pathway.Overexpression of TRIM59 in vivo effectively reduced the expressions of MDA, CK, and LDH, and increased the expression of SOD and the activity of Na+-K+-ATPase and Ca2+-Mg2+-ATPase. In addition, overexpression of TRIM59 in H9c2 cells significantly reduced the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative stress (ROS) levels. TRIM59 also significantly increased the activity of PI3K/Akt signaling pathway and promoted the phosphorylation of Akt.TRIM59 reduces the level of inflammation and apoptosis of myocardial cells caused by MIRI by activating the PI3K/Akt signaling pathway, thereby reducing myocardial injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI