医学
药理学
再灌注损伤
TFAM公司
尼泊尔卢比1
过氧化物酶体增殖物激活受体
缺血
心肌缺血
心脏病学
汤剂
心肌保护
罗格列酮
内科学
受体
化学
线粒体
生物化学
线粒体生物发生
作者
Fei Lin,Yuqing Tan,Xuanhui He,Lili Guo,Wei Benjun,Junping Li,Zhong Chen,Hengwen Chen,Jie Wang
标识
DOI:10.3389/fphar.2020.546825
摘要
HXHT can reduce myocardial I/R injury in hyperlipidemic rats. The protective mechanisms may involve a reduction in blood lipids, enhancement of PGC-1α-PPARα pathway activity, and, subsequently, an increase in fatty acid β-oxidation, which may provide the required input for mitochondrial energy metabolism. HXHT can additionally enhance PGC-1α-NRF1-mtTFA pathway activity and, subsequently, increase the antioxidant capacity, promote mtDNA synthesis, and reduce mitochondrial damage. The two pathways use PGC-1α as the intersection point to protect mitochondrial structure and function, reduce I/R-induced injury, and improve cardiac function.
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