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Ginsenoside Rg1 modulation on thrombospondin‐1 and vascular endothelial growth factor expression in early renal fibrogenesis in unilateral obstruction
Author(s) -
Xie XiSheng,
Liu HengChuan,
Wang FengPing,
Zhang ChengLong,
Zuo Chuan,
Deng Yao,
Fan JunMing
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3190
Subject(s) - kidney , peritubular capillaries , fibrosis , vascular endothelial growth factor , ginsenoside rg1 , kidney disease , endocrinology , medicine , angiogenesis , pathology , ginsenoside , vegf receptors , ginseng , alternative medicine
Abstract Renal interstitial fibrosis is the major histopathological change seen in a variety of renal disorders and is closely related to renal dysfunction. Progressive interstitial fibrosis accompanied by the loss of renal tubules and interstitial capillaries typifies all progressive renal disease. Thrombospondin‐1 (TSP‐1) is a major angiogenic inhibitor. It is demonstrated that TSP‐1 levels were correlated with the loss of glomerular and peritubular capillaries and TSP‐1 could promote renal scarring by effects on the endothelium. It has been reported that ginsenoside Rg1 inhibited renal interstitial fibrosis in rats via suppressing the expression of TSP‐1. The present study was designed to examine whether ginsenoside Rg1 could modulate the integrity of the microvasculature and hence affect the progression of renal fibrosis in a rat unilateral ureteral obstruction (UUO) model. In UUO control kidneys, associated with interstitial fibrosis, lower peritubular capillary densities were prominent. These changes were all improved by ginsenoside Rg1 treatment. Interestingly, ginsenoside Rg1 decreased the expression of TSP‐1 and enhanced vascular endothelial growth factor (VEGF) expression. The results show for the first time that ginsenoside Rg1 can evidently inhibit renal interstitial fibrosis in rats with UUO. The mechanism might be related to suppression of the expression of TSP‐1 and to repair of the peritubular capillary. Copyright © 2010 John Wiley & Sons, Ltd.