| Literature DB >> 26661649 |
Kyung Don Ju1, Hyo Jin Kim2, Bodokhsuren Tsogbadrakh1, Jinho Lee1, Hyunjin Ryu2, Eun Jin Cho2, Young-Hwan Hwang3, Kiwon Kim4, Jaeseok Yang5, Curie Ahn5, Kook-Hwan Oh6.
Abstract
HL156A is a novel AMP-activated protein kinase (AMPK) activator. We aimed to investigate the protective mechanism of HL156A against peritoneal fibrosis (PF) in in vivo and in vitro models. The rat PF model was induced by daily intraperitoneally injection of chlorhexidine (CHX) solution containing 0.1% CHX gluconate and 15% ethanol for 4 wk. The rats in the treatment group were treated with HL156A (1 mg·kg(-1)·day(-1)). Control rats were injected with vehicle alone. In vitro, cultured rat peritoneal mesothelial cells (RPMCs) were treated with either high glucose (HG; 50 mM), normal glucose (NG; 5 mM), NG+HL156A, or HG+HL156A. HL156A in supplemented rats ameliorated peritoneal calcification, cocoon formation, bowel obstruction, and PF. Immunohistochemistry showed reduced fibronectin accumulation in the peritoneum of HL156A-treated rats compared with those injected with CHX alone. HL156A treatment of RPMCs inhibited HG-induced myofibroblast transdifferentiation and markers of epithelial-mesenchymal transition (EMT). Moreover, HL156A ameliorated HG-induced transforming growth factor-β1, Smad3, Snail, and fibronectin expression in the RPMCs via AMPK upregulation. These results suggest that HL156A exhibits a protective effect in PF progression. Further research is warranted to seek the therapeutic potential of HL156A as an antifibrotic agent in peritoneal dialysis patients.Entities:
Keywords: AMP kinase; HL156A; epithelial-mesenchymal transition (EMT); fibronectin; peritoneal fibrosis
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Year: 2015 PMID: 26661649 DOI: 10.1152/ajprenal.00204.2015
Source DB: PubMed Journal: Am J Physiol Renal Physiol ISSN: 1522-1466