Study on effect of fushenkeli on expression of TAK1 in human renal tubular epithelial cells and its possible mechanism.
- Author:
Minglong LIU
1
;
Yongxiang ZENG
;
Shouyan LU
;
Jianhua LI
;
Tianxi LIU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Cell Proliferation; drug effects; Collagen Type IV; drug effects; metabolism; Drugs, Chinese Herbal; pharmacology; Epithelial Cells; drug effects; metabolism; Humans; Kidney Tubules; cytology; MAP Kinase Kinase Kinases; drug effects; metabolism; RNA, Messenger; drug effects; metabolism; Transforming Growth Factor beta1; administration & dosage
- From: China Journal of Chinese Materia Medica 2011;36(18):2571-2575
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of fushenkeli on the expression of TAK1 in the proliferation of the renal tubular epithelial cells induced by TGF-beta1 and its possible mechanism.
METHODHuman renal tubular epithelial (HK-2) cells were divided into five groups:blank control group, TGF-beta1 group (5 microg x L(-1)), intervention group 1 (5 microg x L(-1) of TGF-beta1 + 100 mg x L(-1) of fushenkeli), intervention group 2 (5 microg x L(-1) of TGF-beta1 + 500 mg x L(-1) of fushenkeli) and intervention group 3 (5 microg x L(-1) of TGF-beta1 + 1 g x L(-1) of fushenkeli). HK-2 proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay. Type IV collagen in the supernatants of the cultured HK-2 was detected by ELISA at 12, 24, 48 hours respectively. The protein and mRNA expressions of TAK1 was measured by Western blot and real-time quantitative PCR.
RESULT1) The cell proliferation and the expression of type IV collagen were increased compared with the control group (P<0.05, P<0.01), but they were decreased in intervention group. 2) The expressions of protein and mRNA of TAK1 in TGF-beta1 group were upregulating significantly compared with control group (P<0.01), but they were downregulating in intervention group, especially in intervention group 3.
CONCLUSIONFushenkeli could inhibits TAK1 expression induced by TGF-beta1 in the proliferation of HK-2 cell.
