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在高脂肪饮食喂养的小鼠中,连接蛋白-2 参与鸢尾素对缺血再灌注诱导的肝损伤的保护作用。

Involvement of kindlin-2 in irisin's protection against ischaemia reperfusion-induced liver injury in high-fat diet-fed mice.

机构信息

National Local Joint Engineering Research Center for Precision Surgery & Regenerative Medicine, Shaanxi Provincial Center for Regenerative Medicine and Surgical Engineering, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Department of Hepatobiliary Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

出版信息

J Cell Mol Med. 2020 Nov;24(22):13081-13092. doi: 10.1111/jcmm.15910. Epub 2020 Sep 20.

Abstract

Liver steatosis is associated with increased ischaemia reperfusion (I/R) injury. Our previous studies have shown that irisin, an exercise-induced hormone, mitigates I/R injury via binding to αVβ5 integrin. However, the effect of irisin on I/R injury in steatotic liver remains unknown. Kindlin-2 directly interacts with β integrin. We therefore suggest that irisin protects against I/R injury in steatotic liver via a kindlin-2 dependent mechanism. To study this, hepatic steatosis was induced in male adult mice by feeding them with a 60% high-fat diet (HFD). At 12 weeks after HFD feeding, the mice were subjected to liver ischaemia by occluding partial (70%) hepatic arterial/portal venous blood for 60 minutes, which was followed by 24 hours reperfusion. Our results showed HFD exaggerated I/R-induced liver injury. Irisin (250 μg/kg) administration at the beginning of reperfusion attenuated liver injury, improved mitochondrial function, and reduced oxidative and endoplasmic reticulum stress in HFD-fed mice. However, kindlin-2 inhibition by RNAi eliminated irisin's direct effects on cultured hepatocytes. In conclusion, irisin attenuates I/R injury in steatotic liver via a kindlin-2 dependent mechanism.

摘要

肝脂肪变性与缺血再灌注(I/R)损伤增加有关。我们之前的研究表明,运动诱导的激素鸢尾素通过与αVβ5 整合素结合来减轻 I/R 损伤。然而,鸢尾素对脂肪变性肝脏的 I/R 损伤的影响尚不清楚。Kindlin-2 直接与β整合素相互作用。因此,我们认为鸢尾素通过依赖于 Kindlin-2 的机制来保护脂肪变性肝脏免受 I/R 损伤。为了研究这一点,通过用 60%高脂肪饮食(HFD)喂养雄性成年小鼠来诱导肝脂肪变性。在 HFD 喂养 12 周后,通过阻断部分(70%)肝动脉/门静脉血流 60 分钟来使小鼠发生肝缺血,随后进行 24 小时再灌注。我们的结果表明 HFD 加重了 I/R 引起的肝损伤。再灌注开始时给予鸢尾素(250μg/kg)可减轻 HFD 喂养小鼠的肝损伤,改善线粒体功能,并减少氧化应激和内质网应激。然而,RNAi 抑制 Kindlin-2 消除了鸢尾素对培养肝细胞的直接作用。总之,鸢尾素通过依赖于 Kindlin-2 的机制减轻脂肪变性肝脏的 I/R 损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4646/7701503/9972d20cc654/JCMM-24-13081-g001.jpg

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