Proliferation and activation of acetaldehyde-induced HSC-T6 cells through RNA inference targeting adenosine A1 and A2 A receptors
10.3969/j.issn.1001-1978.2015.01.012
- VernacularTitle:RNAi介导大鼠腺苷A1和A2 A受体基因沉默对乙醛诱导的肝星状细胞活化增殖的影响
- Author:
Qi WANG
;
He WANG
;
Ling RAO
;
Han ZHAO
;
Feng YANG
;
Yan YANG
;
Xiongwen Lü
;
Jun LI
- Publication Type:Journal Article
- Keywords:
adenosine A1 receptor;
adenosine A2 A receptor;
hepatic stellate cell;
cell proliferation;
acetal-dehyde;
alcoholic liver fibrosis
- From:
Chinese Pharmacological Bulletin
2015;(1):50-54,55
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the influence of down-regulating adenosine A1 receptor and adenosine A2 A receptor gene expression on proliferation and activation of acetaldehyde-induced hepatic stellate cell-T6 cells through siRNA. Methods Alcoholic liver fibrosis in vitro model was constructed by inducing HSC-T6 cells with acetaldehyde. siRNA targeting A1R and A2AR were designed and synthesized according to its mRNA. The siRNA was transfected into rat HSC-T6 cells by li-posome LipofectamineTM 2000. HSC cell proliferation was measured by MTT. The mRNA levels of A1R, A2AR, α-SMA, Collagen I in the supernatant of the cell culture were measured by Quantitative Real-Time PCR. The protein levels of A1R, A2AR, α-SMA, Collagen I were measured by Western blot. Results A1 R and A2 AR siRNA effectively inhibited the cell proliferation, and they also significantly decreased the levels of A1R, A2AR,α-SMA, Collagen I, suggesting that A1 R and A2 AR might be potential target genes in the alcoholic liver fibrosis. Conclusions Silencing A1 R or A2 AR by RNAi can significantly inhibit the HSC proliferation, A1R and A2AR may be potential therapeutic target genes for alcoholic liver fibrosis.
