Irisin alleviates liver ischemia-reperfusion injury by inhibiting excessive mitochondrial fission, promoting mitochondrial biogenesis and decreasing oxidative stress.

Irisin alleviates liver ischemia-reperfusion injury by inhibiting excessive mitochondrial fission, promoting mitochondrial biogenesis and decreasing oxidative stress.
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鸢尾素通过抑制线粒体过度裂变、促进线粒体生物发生和减少氧化应激来减轻肝脏缺血再灌注损伤

DOI:
10.1016/j.redox.2018.10.019
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发表时间:
2019-01
期刊:
影响因子:
11.4
通讯作者:
Wu R
Wu R
中科院分区:
生物学1区
文献类型:
--
作者:
Bi J;Zhang J;Ren Y;Du Z;Li Q;Wang Y;Wei S;Yang L;Zhang J;Liu C;Lv Y;Wu R

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目前对肝脏缺血再灌注损伤的治疗主要是支持性治疗,没有特异性治疗方法。Irisin是一种新近发现的激素,在能量消耗和氧化代谢中起着关键作用;然而,Irisin是否对肝I/R损伤有任何保护作用仍不清楚。在本研究中,我们发现肝I/R后24小时血清和肝中鸢尾素水平显著降低。外源性鸢尾素治疗可改善肝功能,减少肝坏死和细胞凋亡,减轻肝I/R后的炎症反应。同时,外源性Irisin可显著抑制肝I/R线粒体分裂相关蛋白dynamin related protein 1(drp-1)和fis 1(Fis-1)的表达。此外,外源性鸢尾素处理增加了线粒体含量,并增加了线粒体生物发生相关的过氧化物酶体增殖激活受体γ(PPARγ)共激活因子1α(PGC-1α)和线粒体转录因子(TFAM)的表达。此外,鸢尾素通过上调解偶联蛋白(UCP)2在肝I/R中的表达来降低氧化应激。结果表明,外源性鸢尾素通过抑制线粒体分裂、促进线粒体生物合成和减轻氧化应激而减轻肝I/R损伤。Irisin治疗肝I/R损伤似乎是一种新的和有前途的治疗方法。Irisin保护肝细胞免受缺血/再灌注(I/R)诱导的损伤。Irisin抑制肝I/R后线粒体过度分裂。Irisin促进肝I/R后线粒体生物合成Irisin降低肝I/R后的氧化应激。
Current management of liver ischemia-reperfusion (I/R) injury is mainly based on supportive care and no specific treatment is available. Irisin, a recently identified hormone, plays pivotal roles in energy expenditure and oxidative metabolism; however, it remains unknown whether irisin has any protective effects on hepatic I/R injury. In this study, we found that serum and liver irisin levels were markedly decreased at 24 h after hepatic I/R. Treatment with exogenous irisin improved liver function, reduced liver necrosis and cell apoptosis, and relieved inflammatory response after hepatic I/R. Meanwhile, exogenous irisin markedly inhibited mitochondrial fission related protein dynamin related protein 1 (drp-1) and fission 1 (Fis-1) expression in hepatic I/R. Additionally, treatment with exogenous irisin increased mitochondrial content and increased mitochondrial biogenesis related peroxisome proliferative activated receptor-γ (PPARγ) co-activator 1α (PGC-1α) and mitochondrial transcription factor (TFAM) expression. Furthermore, irisin decreased oxidative stress by upregulating uncoupling proteins (UCP) 2 expression in hepatic I/R. The results reveal that treatment with exogenous irisin alleviated hepatic I/R injury by restraining mitochondrial fission, promoting mitochondrial biogenesis and relieving oxidative stress. Irisin treatment appears to be a novel and promising therapeutic approach for hepatic I/R injury. Irisin protects hepatocytes against ischemia/reperfusion (I/R)-induced injury. Irisin inhibits excessive mitochondrial fission after hepatic I/R. Irisin promotes mitochondrial biogenesis after hepatic I/R. Irisin reduces oxidative stress after hepatic I/R.
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发表时间: 2015
影响因子: --
作者:
Cursio R;Colosetti P;Gugenheim J
通讯作者: Gugenheim J
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