Protective effect of ghrelin on intestinal I/R injury in rats.

IF 1.6
Open medicine (Warsaw, Poland) Pub Date : 2022-07-20 eCollection Date: 2022-01-01 DOI:10.1515/med-2022-0520
Meng Jiang, Shengxia Wan, Xiaoyong Dai, Youwen Ye, Wei Hua, Guoguang Ma, Xiufeng Pang, Huanhuan Wang, Bin Shi
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Abstract

This study aimed to investigate whether ghrelin affected the autophagy and inflammatory response of intestinal intraepithelial lymphocytes (IELs) by regulating the NOD2/Beclin-1 pathway in an intestinal ischemia-reperfusion (I/R) injury model. Twenty hours after implementing the intestinal I/R injury rat model, the small intestine and both lungs were collected for histological analysis. The morphological changes in the intestinal mucosa epithelium and lung tissues were evaluated using hematoxylin-eosin staining. The activity of autophagic vacuoles and organ injury were evaluated using electron microscopy. The cytokine levels (IL-10 and TNF-α) in IEL cells and lung tissue were determined using enzyme-linked immunosorbent assay. RT-qPCR and western blot assays were conducted to check the NOD2, Beclin-1, and ATG16 levels. Ghrelin relieved the I/R-induced destruction of the intestinal mucosa epithelium and lung tissues. Moreover, ghrelin enhanced autophagy in the intestinal epithelium and lungs of I/R rats. In addition, the levels of autophagy-associated proteins (Beclin-1, ATG16, and NOD2) were higher in the ghrelin treatment group than in rats with I/R. Ghrelin reduced significantly the IL-10 and TNF-α levels. However, these changes were reversed by the NOD2 antagonist. In conclusion, ghrelin may relieve I/R-induced acute intestinal mucosal damage, autophagy disorder, and inflammatory response in IELs by regulating the NOD2/Beclin-1 pathway.

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胃饥饿素对大鼠肠I/R损伤的保护作用。
本研究旨在探讨在肠缺血再灌注(I/R)损伤模型中,ghrelin是否通过调节NOD2/Beclin-1通路影响肠上皮内淋巴细胞(IELs)的自噬和炎症反应。建立肠I/R损伤大鼠模型20 h后,取小肠和双肺进行组织学分析。苏木精-伊红染色观察肠黏膜上皮和肺组织的形态学变化。电镜观察自噬空泡活性和器官损伤情况。采用酶联免疫吸附法测定IEL细胞和肺组织中细胞因子(IL-10、TNF-α)水平。RT-qPCR和western blot检测NOD2、Beclin-1和ATG16的表达水平。Ghrelin减轻了I/ r诱导的肠黏膜上皮和肺组织的破坏。此外,胃饥饿素还能增强I/R大鼠肠上皮和肺的自噬。此外,胃饥饿素治疗组的自噬相关蛋白(Beclin-1、ATG16和NOD2)水平高于I/R大鼠。Ghrelin显著降低IL-10和TNF-α水平。然而,这些变化被NOD2拮抗剂逆转。综上所述,ghrelin可能通过调节NOD2/Beclin-1通路,缓解I/ r诱导的急性肠黏膜损伤、自噬障碍和IELs炎症反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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