Astragalosides IV inhibits high glucose-induced cell apoptosis through HGF activation in cultured human tubular epithelial cells

• Published in: Renal failure Vol. 36; no. 3; pp. 400 - 406
• Main Authors: Wang, Qin, Shao, Xinghua, Xu, Weijia, Qi, Chaojun, Gu, Leyi, Ni, Zhaohui, Mou, Shan
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare USA, Inc 01.04.2014; Taylor & Francis
• Subjects: Apoptosis - drug effects; Astragalosides IV; cell apoptosis; Cell Survival - drug effects; Cells, Cultured; Dose-Response Relationship, Drug; Drugs, Chinese Herbal - administration & dosage; Drugs, Chinese Herbal - pharmacology; Enzyme Activation - drug effects; Epithelial Cells; Glucose - administration & dosage; hepatocyte growth factor; Hepatocyte Growth Factor - secretion; Humans; Kidney Tubules, Proximal - drug effects; Kidney Tubules, Proximal - pathology; MAPK signaling pathway; p38 Mitogen-Activated Protein Kinases - metabolism; Saponins - administration & dosage; Saponins - pharmacology; Signal Transduction; Transforming Growth Factor beta - secretion; Triterpenes - administration & dosage; Triterpenes - pharmacology; tubular epithelial cells
• ISSN: 0886-022X; 1525-6049
• DOI: 10.3109/0886022X.2013.867798

Abstract Astragaloside IV (ASI) in Radix Astragali 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.