Astragalosides IV inhibits high glucose-induced cell apoptosis through HGF activation in cultured human tubular epithelial cells. (April 2014)

• Record Type: Journal Article
• Authors: Wang, Qin; Shao, Xinghua; Xu, Weijia; Qi, Chaojun; Gu, Leyi; Ni, Zhaohui; Mou, Shan
• Is Part Of: Renal failure. Volume 36:Number 3(2014)
• Page Start: 400
• Page End: 406
• Publication Date: 2014-04
• Subjects: Chronic renal failure -- Periodicals; Acute renal failure -- Periodicals; Uremia -- Periodicals; 616.614005
• DOI: 10.3109/0886022X.2013.867798
• Languages: English
• ISSNs: 0886-022X

Abstract

<abstract> <title>Abstract</title> <p>Astragaloside IV (ASI) in <italic>Radix Astragali</italic> is believed to be the active component. The study aims to investigate whether ASI inhibits tubular epithelial cells apoptosis induced by high glucose and its mechanisms. Tubular epithelial cells in this paper were isolated from human kidney. The cells apoptosis was detected by TUNEL and caspase 3 assay. The protein levels of HGF and TGF-β1 were measured by ELISA. The phospho-p38 production, ERK and JNK were determined by Western blot. ASI could inhibit cells apoptosis induced by high glucose (25 mmol/L) in dose-dependent and time-dependent manners. ASI also inhibited high glucose-induced expression of TGF-β1 and activation of p38 MAPK pathway at the protein level. Furthermore, ASI increased HGF production in human tubular epithelial cells. The ASI inhibition of tubular epithelial cells apoptosis and reduction of TGF-β1 expression induced by high glucose may represent a new treatment for diabetic kidney injury. The mechanism underlying this inhibitory effect may be related to the inhibition of p38 MAPK signaling pathway activation and HGF overproduction.</p> </abstract>