Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition.
- Author:
Rui-fang ZHANG
1
;
Jian-xin WAN
;
Yan-fang XU
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Cadherins; metabolism; Cell Differentiation; drug effects; Cell Line; Cholestenones; pharmacology; Complement C3a; metabolism; Epithelial Cells; drug effects; metabolism; Epithelial-Mesenchymal Transition; drug effects; Humans; Kidney Tubules; cytology; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(10):1407-1412
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study whether alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT).
METHODSThe in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol alisol B, respectively. The mRNA and protein expressions of alpha-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively.
RESULTSThe mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P < 0.01), the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously enhanced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P < 0.01). When compared with the group intervened by exogenous C3a, after intervention of alisol B, the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously reduced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously increased (P < 0.05).
CONCLUSIONSExogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.
