Inhibitory effect of chailing decoction on renal tubular epithelial phenotype transformation in rats with cyclosporine A-induced nephropathy.
- Author:
Xiang-ting WANG
1
;
Min WEI
;
Xia WANG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Animals; Collagen Type III; metabolism; Cyclosporine; adverse effects; Drugs, Chinese Herbal; pharmacology; Epithelial Cells; metabolism; Fibrosis; Kidney Diseases; chemically induced; metabolism; pathology; Kidney Tubules; drug effects; metabolism; pathology; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta1; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2011;31(1):94-98
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of Chailing Decoction (CLD) on alpha-smooth muscular actin (alpha-SMA, a marker of renal tubular epithelial phenotype transformation) in rats with cyclosporine A (CsA)-induced nephropathy for investigate its mechanism of action in inhibiting tubulo-interstitial fibrosis.
METHODSForty Sprague-Dawley rats were equally randomized into four groups: the normal group, the model group, the positive control group and the Chinese medicine (CM) group. Excepting those in the normal group received gastrogavage with olive oil, rats in the other three groups were made into nephropathy model by oral infusion of CsA 30 mg/ (kg x d) for 28 days. At the same time of modeling, rats in the positive control and CM groups were treated respectively with Valsartan 10 mg/(kg x d) and CLD 3 g/(kg x d). The mRNA and protein expressions of alpha-SMA in rats' kidney were detected by RT-PCR, Western blot, immunohistochemical and flow cytometry, and the mRNA expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type III (Col III) were determined by RT-PCR.
RESULTSLevels of (alpha-SMA, TGF-beta1, and Col III were significantly higher in the model group than those in the normal group respectively (P < 0.01 or P < 0.05), and the high levels were down-regulated in the positive control and CM groups after treatment (P < 0.01 or P < 0.05).
CONCLUSIONCLD could retard the progress of renal interstitial fibrosis by way of inhibiting renal tubular epithelial phenotype transformation.