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胱抑素对动脉粥样硬化性肾损害的治疗作用

Therapeutic Effect of Cystatin on Atherosclerotic Renal Damage.

作者信息

Yang Huijuan, Li Hongqi, Chen Weidong, Mei Zhijie, Yuan Yuan, Wang Xiaoli, Chu Liang, Xu Yu, Sun Yan, Li Dingru, Gao Hongyu, Zhan Bin, Li Huihui, Yang Xiaodi

机构信息

Department of Nephrology, First Affiliated Hospital of Bengbu Medical College, Bengbu, China.

Anhui Key Laboratory of Infection and Immunity of Bengbu Medical College, Bengbu, China.

出版信息

Front Cell Dev Biol. 2021 Nov 25;9:760980. doi: 10.3389/fcell.2021.760980. eCollection 2021.

DOI:10.3389/fcell.2021.760980
PMID:34901005
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8656285/
Abstract

Atherosclerosis is a chronic inflammation of the arterial vessel wall driven by lipid metabolism disorders. Although helminthic infection and their derivatives have been identified to attenuate the chronic inflammatory diseases, the immunomodulatory effect of recombinant cystatin (r-Cys) on metabolic diseases and atherosclerosis has not been reported. In this study, we investigated the therapeutic efficacy of r-Cys on atherosclerotic renal damage and explored the related immunological mechanism. The results demonstrated that treatment with rCys significantly reduced body weight gain, hyperlipidemia, and atherosclerosis induced by the high-fat diet in apoE mice. The treatment of r-Cys also significantly improved kidney functions through promoting macrophage polarization from M1 to M2, therefore inhibiting M1 macrophage-induced inflammation. The possible mechanism underlying the regulatory effect of r-Cys on reducing atherosclerosis and atherosclerotic renal damage is that r-Cys stimulates regulatory T cell and M2 macrophage polarization that produce regulatory cytokines, such as interleukin 10 and transforming growth factor β. The therapeutic effect of r-Cys on atherosclerotic renal damage is possibly through inhibiting the activation of TLR2/Myd88 signaling pathway. The results in this study provide evidence for the first time that -derived cystatin could be developed as a therapeutic agent to treat lipid metabolism disorder and atherosclerosis that threats million lives around the world.

摘要

动脉粥样硬化是一种由脂质代谢紊乱驱动的动脉血管壁慢性炎症。尽管已发现蠕虫感染及其衍生物可减轻慢性炎症性疾病，但重组胱抑素（r-Cys）对代谢性疾病和动脉粥样硬化的免疫调节作用尚未见报道。在本研究中，我们研究了r-Cys对动脉粥样硬化性肾损伤的治疗效果，并探讨了相关的免疫机制。结果表明，rCys治疗可显著降低apoE小鼠高脂饮食诱导的体重增加、高脂血症和动脉粥样硬化。r-Cys治疗还通过促进巨噬细胞从M1向M2极化，从而抑制M1巨噬细胞诱导的炎症，显著改善肾功能。r-Cys降低动脉粥样硬化和动脉粥样硬化性肾损伤的调节作用的可能机制是r-Cys刺激产生调节性细胞因子（如白细胞介素10和转化生长因子β）的调节性T细胞和M2巨噬细胞极化。r-Cys对动脉粥样硬化性肾损伤的治疗作用可能是通过抑制TLR2/Myd88信号通路的激活。本研究结果首次提供了证据，表明源自[此处原文可能有误，推测可能是某种生物]的胱抑素可开发为治疗脂质代谢紊乱和动脉粥样硬化的治疗药物，而动脉粥样硬化威胁着全球数百万人的生命。

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Therapeutic inhibition of miR-802 protects against obesity through AMPK-mediated regulation of hepatic lipid metabolism.
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