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通过Nrf2介导的HO-1激活对氧化应激诱导的骨骼肌L6成肌细胞损伤的预防作用。

The preventive effect of on oxidative stress-induced cellular damage in skeletal L6 myoblasts through Nrf2-mediated activation of HO-1.

作者信息

Park Cheol, Lee Hyesook, Kim Sung Ok, Lee Eun-Woo, Lee Hyun-Tai, Kwon Hyun Ju, Kim Byung Woo, Kim Gi-Young, Kim Mi Ryeo, Choi Yung Hyun

机构信息

Division of Basic Sciences, College of Liberal Studies, Dong-eui University, Busan, 47340 Republic of Korea.

Anti-Aging Research Center, Dong-eui University, Busan, 47340 Republic of Korea.

出版信息

Toxicol Res. 2022 Jul 22;39(1):25-36. doi: 10.1007/s43188-022-00141-5. eCollection 2023 Jan.

Abstract

The aim of the present study is to investigate the preventive effect of water extract of (MRWE) on oxidative stress-mediated cellular damages in rat skeletal L6 myoblasts. Our results demonstrated that MRWE pretreatment markedly improved cell survival and suppressed cell cycle arrest at the G2/M phase and apoptosis in hydrogen peroxide (HO)-treated L6 cells. HO-triggered DNA damage was also notably reduced by MRWE, which since it was correlated with protection of reactive oxygen species (ROS) production. Additionally, HO stimulated cytosolic release of cytochrome and up-regulation of Bax/Bcl-2 ratio, whereas MRWE suppressed these changes following by HO. Moreover, MRWE inhibited the cleavage of poly(ADP-ribose) polymerase as well as the activity of caspase-3 by HO. Furthermore, MRWE enhanced HO-mediated expression of nuclear factor erythroid 2-associated factor 2 (Nrf2) and its representative downstream enzyme, heme oxygenase-1 (HO-1). However, the protective effects of MRWE on HO-induced ROS production, cell cycle arrest and apoptosis were significantly attenuated by HO-1 inhibitor. In conclusion, our present results suggests that MRWE could protect L6 myoblasts from HO-induced cellular injury by inhibiting ROS generation along with Nrf2-mediated activation of HO-1, indicating this finding may expand the scope of application of in medicine.

摘要

本研究的目的是探讨(此处原文缺失具体物质名称)水提取物(MRWE)对大鼠骨骼肌L6成肌细胞氧化应激介导的细胞损伤的预防作用。我们的结果表明,MRWE预处理显著提高了细胞存活率,抑制了过氧化氢(HO)处理的L6细胞在G2/M期的细胞周期阻滞和细胞凋亡。MRWE还显著降低了HO引发的DNA损伤,这与对活性氧(ROS)产生的保护作用相关。此外,HO刺激了细胞色素c的胞质释放以及Bax/Bcl-2比值的上调,而MRWE抑制了HO处理后的这些变化。此外,MRWE抑制了HO诱导的聚(ADP-核糖)聚合酶的裂解以及caspase-3的活性。此外,MRWE增强了HO介导的核因子红细胞2相关因子2(Nrf2)及其代表性下游酶血红素加氧酶-1(HO-1)的表达。然而,HO-1抑制剂显著减弱了MRWE对HO诱导的ROS产生、细胞周期阻滞和细胞凋亡的保护作用。总之,我们目前的结果表明,MRWE可以通过抑制ROS生成以及Nrf2介导的HO-1激活来保护L6成肌细胞免受HO诱导的细胞损伤,表明这一发现可能会扩大(此处原文缺失具体物质名称)在医学上的应用范围。

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