Actoeside mitigated the renal proximal tubule cells damage triggered by high glucose through miR-766/VCAM1/NF-κB signalling pathway.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2023-12-01 Epub Date: 2021-08-02 DOI:10.1080/13813455.2021.1920983

Xiaodong Zhao, Honglei Hu, Kun Sun, Wenlong Liang, Zhenzhen Wang, Xingqian Jin, Shujuan Wang

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引用次数: 0

Abstract

Context: Diabetic nephropathy (DN) triggered by diabetes mellitus is one of the primary causes of end-stage renal failure worldwide.

Objective: This study intends to explore the function and potential mechanism of actoeside on renal proximal tubule (HK-2) cells damage induced by high-glucose (HG).

Methods: The DN model was established in HK-2 cells with 30 mM HG treatment. The viability, apoptosis and inflammation of HK-2 cells were analysed severally via CCK-8, flow cytomery and ELISA. The key factors related to NF-κB were detected by western blotting.

Results: Actoeside attenuated the HG-induced HK-2 cells damage. The differentially expression of miR-766 and VCAM1 in DN patients was reversed by actoeside. Moreover, the increased phosphorylation levels of p65 NF-κB/IκBα induced by HG were attenuated by actoeside.

Conclusions: Actoeside promoted the growth and repressed the apoptosis and inflammation of HK-2 cells via miR-766/VCAM1/NF-κB signalling pathway, affording a promising idea for the treatment of DN.

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actoside通过miR-766/VCAM1/NF-κB信号通路减轻高糖引发的肾近端小管细胞损伤。

背景:糖尿病引发的糖尿病肾病(DN)是世界范围内终末期肾功能衰竭的主要原因之一。目的:探讨牛蒡苷对高糖(HG)所致肾近端小管(HK-2)细胞损伤的作用及可能机制。方法:采用30 mM HG处理HK-2细胞，建立DN模型。采用CCK-8、流式细胞术、ELISA检测HK-2细胞活力、凋亡及炎症反应。western blot检测与NF-κB相关的关键因子。结果:乙酰胆碱能减轻hg诱导的HK-2细胞损伤。通过actoside逆转miR-766和VCAM1在DN患者中的差异表达。此外，HG诱导的p65 NF-κB/ i -κB α磷酸化水平升高被乙酰胆碱抑制。结论:actoside通过miR-766/VCAM1/NF-κB信号通路促进HK-2细胞生长，抑制细胞凋亡和炎症反应，为治疗DN提供了良好的思路。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.