Effect of Astragalus mongholicus on expression of transforming growth factor- beta1 in SD rats with unilateral ureteral occlusion.
- Author:
Chuan ZUO
1
;
Xisheng XIE
;
Yao DENG
;
Junming FAN
Author Information
- Publication Type:Journal Article
- MeSH: Actins; genetics; Animals; Astragalus Plant; chemistry; Drugs, Chinese Herbal; pharmacology; Gene Expression Regulation; drug effects; Kidney Tubules; drug effects; metabolism; Male; RNA, Messenger; genetics; metabolism; Rats; Transforming Growth Factor beta1; genetics; Ureteral Obstruction; metabolism; pathology; prevention & control
- From: China Journal of Chinese Materia Medica 2009;34(2):193-198
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of Astragalus mongholicus (AM) on the expression of transforming growth factor-beta1 (TGF-beta1) in SD rats with unilateral ureteral occlusion (UUO) and to elucidate the mechanisms underlying the renoprotective effects of AM.
METHODFifty-four Sprague-Dawley rats were randomly divided into 4 groups: sham-operation group, the UUO group and AM treatment group. After administration of AM (10 g kg(-1) d(-1)) for 3, 7 and 14 days, the dynamic histological changes of renal interstitial tissues were observed and renal damage including tubular impairment and interstitial fibrosis were quantified on HE and Masson stained tissue sections. The expression of TGF-beta1 and alpha-smooth muscle actin (alpha-SMA) was measured by immunohistochemistry staining sections. The mRNA of TGF-beta1 and alpha-SMA were reverse transcribed and quantified by real-time PCR. The expression of TGF-beta1 protein were assessed by Western blot.
RESULTRenal damage was exacerbated and the expression of alpha-SMA and TGF-beta1 were all significantly increased in UUO group compared with those of sham-operation group (P<0.05) at each time point. Tubular impairment and interstitial fibrosis were alleviated, and up-regulations of expressions of TGF-beta1 and alpha-SMA were significantly suppressed by AM treatment (P<0.05).
CONCLUSIONAM can ameliorate renal interstitial fibrosis induced by UUO in vivo. The mechanisms of its antifibrotic effects might be related with the down-regulation of TGF-beta1 expression and suppression of tubular epithelial myofibroblast transdifferentiation in the progress of renal interstitial fibrosis.