Ginsenoside Rg1, a major active component isolated from Panax notoginseng, restrains tubular epithelial to myofibroblast transition in vitro.
The medicinal herb, Panax notoginseng, has been used for thousands of years in traditional Chinese medicine and possesses anti-fibrosis properties. Epithelial-myofibroblast transition (EMT) plays an important role in renal tubulointerstitial fibrosis. The present study was designed to examine whether ginsenoside Rg1, a major active component isolated from Panax notoginseng, has an ability to block this phenotypic transition in rat renal tubular epithelial cells (NRK-52E) induced by transforming growth factor-beta1 (TGF-beta1). The morphology of tubular epithelial-myofibroblast transition was observed through light microscope and transmission electron microscopy. alpha-SMA and E-cadherin are two markers of tubular epithelial-myofibroblast transition, their protein expressions were assessed by immunohistochemistry and western blot analysis. Gene expression of alpha-SMA as well as the two major extracellular matrix components collagen I and fibronectin was measured by real-time PCR analysis. Enzyme-linked immunosorbent assay was used to quantitatively detect collagen I and fibronectin in the supernatant. Our results revealed that ginsenoside Rg1 obviously blocked morphologic transformation in NRK-52E induced by TGF-beta1. Meanwhile, ginsenoside Rg1 inhibited the expression of alpha-SMA and the loss of E-cadherin, subsequently decreased the levels of collagen I and fibronectin in a dose-dependent manner. In addition, western blot analysis indicated that ginsenoside Rg1 inhibited the expression of P-ERK1/2 in NRK-52E induced by TGF-beta1. These results suggest that ginsenoside Rg1 can restrain the process of EMT maybe via suppressing the expression of P-ERK1/2 in vitro.
Xie
Xi-Sheng
XS
Department of Nephrology, West China Hospital of Sichuan University, No. 37, Guoxuexiang, Wuhou, Chengdu 610041, China.
Yang
Man
M
Liu
Heng-Chuan
HC
Zuo
Chuan
C
Li
Hui-Juan
HJ
Fan
Jun-Ming
JM
D000199:Actins / Q000378:metabolism; D000818:Animals; D015820:Cadherins / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D024042:Collagen Type I / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects*; D004848:Epithelium / Q000473:pathology*; D005347:Fibroblasts / Q000187:drug effects*; D005353:Fibronectins / Q000378:metabolism; D005355:Fibrosis; D036145:Ginsenosides / Q000494:pharmacology*; D007684:Kidney Tubules / Q000166:cytology*; D048052:Mitogen-Activated Protein Kinase 3 / Q000037:antagonists & inhibitors; D053723:Panax notoginseng / Q000737:chemistry; D010936:Plant Extracts / Q000494:pharmacology*; D018517:Plant Roots; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D053773:Transforming Growth Factor beta1 / Q000009:adverse effects
D000199:Actins; D015820:Cadherins; D024042:Collagen Type I; D005353:Fibronectins; D036145:Ginsenosides; D048052:Mitogen-Activated Protein Kinase 3; D010936:Plant Extracts; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; C498862:Acta2 protein, rat; C035054:ginsenoside Rg1