Anti-fibrotic effects of Salvia miltiorrhiza and Ligustrazine Injection on LX-2 cells involved with increased N-myc downstream-regulated gene 2 expression.
- Author:
Jin ZHENG
1
;
Li-Tian MA
2
;
Qin-You REN
2
;
Yue HU
3
;
Yang BAI
4
;
Huan BIAN
5
;
Yi ZHANG
2
;
Yong-Chun ZHOU
6
;
Ming-Hui YANG
7
Author Information
- Publication Type:Journal Article
- Keywords: N-myc downstream-regulated gene 2; Salvia miltiorrhiza and Ligustrazine Injection; apoptosis; hepatic stellate cell; proliferation
- From: Chinese journal of integrative medicine 2017;23(12):923-928
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of Salvia miltiorrhiza and Ligustrazine Injection (SML) on proliferation and apoptosis of human hepatic stellate cell LX-2 and the expression of N-myc downstreamregulated gene 2 (NDRG2, a tumor suppressor gene).
METHODSHSCs from the LX-2 cell line were cultured in vitro. The proliferative state of different initial LX-2 cell numbers was measured using a 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay. LX-2 cells were plated in 96-well plates at an approximate density of 2.50×10cells/mL and cultured for 24 h followed by the application of different concentrations of SML (1, 2, 4 and 8 μL/mL). Cell proliferation was measured using the MTT assay at 24 and 48 h. Apoptosis was detected by flow cytometry at 24 h. LX-2 cells were treated with different concentrations of SML and extracted with protein lysis buffer. The levels of NDRG2 and β-catenin were measured by Western blot.
RESULTSWith the exception of the 1 and 2 μL/mL concentrations, 4 and 8 μL/mL SML inhibited cell proliferation in a concentration-dependent manner at 24 and 48 h (P<0.05). With the exception of the 1 and 2 μL/mL concentrations, the NDRG2 expression level was greatly increased in a concentration-dependent manner. However, the level of β-catenin was unaffected.
CONCLUSIONSML inhibit LX-2 cell proliferation in a concentration-dependent manner, and the mechanism may be associated with NDRG2 over-expression.