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J Recept Signal Transduct Res. 2016;36(2):152-7. doi: 10.3109/10799893.2015.1061002. Epub 2015 Dec 7.

High glucose induces rat mesangial cells proliferation and MCP-1 expression via ROS-mediated activation of NF-κB pathway, which is inhibited by eleutheroside E.

Author information

1
a Department of Nephrology , Linyi People's Hospital , Linyi , P.R. China .
2
b Department of Endocrinology and Metabolism , The Affiliated Hospital of Qingdao University , Qingdao , P.R. China , and.
3
c Department of Endocrinology , Linyi People's Hospital , Linyi , P.R. China.

Abstract

Glomerular hypertrophy and extracellular matrix accumulation are early features of diabetic nephropathy (DN). High glucose-induced oxidative stress is implicated in the etiology of DN. This study aims to investigate the effect of eleutheroside E (EE) on high glucose mediated rat mesangial cells (MCs) proliferation and monocyte chemoattractant protein-1 (MCP-1) expression and the underlying mechanism. MCs proliferation was assessed by MTT assay. Reactive oxygen species (ROS) level and MCP-1 expression were evaluated by ELISA kit. The protein expression of p47, NF-κB p65, p-NF-κB p65, IκBα, p-IκBα, IKKβ and p-IKKβ were determined by Western blot. The results showed that treatment with EE markedly attenuated high glucose induced MCs proliferation and in a dose-dependent manner. Intervention with EE also significantly blocked high glucose induced intracellular ROS production by decreasing NADPH oxidase activity. Meanwhile, EE administration could effectively alleviate the high glucose-stimulated activation of NF-κB, the degradation of IκBα and the expression of MCP-1. These results demonstrate that high glucose enhances MCs proliferation and MCP-1 expression by activating the ROS/NF-κB pathway and can be inhibited by EE. Our findings provide a new perspective for the clinical treatment of DN.

KEYWORDS:

Cell proliferation; eleutheroside E; high glucose; mesangial cells; monocyte chemoattractant protein-1; nuclear factor kappa B; reactive oxygen species

PMID:
26644089
DOI:
10.3109/10799893.2015.1061002
[Indexed for MEDLINE]

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