氧化应激
再灌注损伤
化学
药理学
心肌再灌注损伤
NF-κB
心肌缺血
缺血
医学
心脏病学
内科学
炎症
作者
Qi Li,Zhuqing Li,Chunlei Liu,Mengping Xu,Tingting Li,Yanxin Wang,Jiaxin Feng,Xuemei Yin,Xiaoyu Du,Chengzhi Lu
标识
DOI:10.1142/s0192415x2350043x
摘要
-insulted cells. Conversely, MA markedly reduced the intranuclear NF-[Formula: see text]B p65 and TNF-[Formula: see text] expression, which could be partially abolished by ML385 (Nrf2 inhibitor). Overall, our results indicate that MA, in a dose-dependent manner, mitigated I/R-induced myocardial injury and oxidative stress via activating the Nrf2/HO-1 pathway and inhibiting NF-[Formula: see text]B activation. Furthermore, MA exerts its cardioprotective effect through regulating the crosstalk between the Nrf2 and NF-[Formula: see text]B pathways.
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