Journal of Practical Hepatology ›› 2022, Vol. 25 ›› Issue (2): 165-169.doi: 10.3969/j.issn.1672-5069.2022.02.004

• Hepatitis in vitro and in mice • Previous Articles     Next Articles

Effects of rosiglitazone on cell proliferation and PPARγ and HO-1 mRNA levels in HSC-T6 cells in vitro

Shi Kourong, Gu Weiying, Liu Juan, et al   

  1. Department of Pharmacy, Seventh People' s Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200137,China
  • Received:2021-05-11 Online:2022-03-10 Published:2022-03-15

Abstract: Objective The aim of this study was to investigate the effects of rosiglitazone (RGZ) on cell proliferation and peroxisome proliferator-activated receptor γ (PPARγ) and heme oxygenase 1 (HO-1) levels in HSC-T6 cells in vitro. Methods The HSC-T6 cells were divided into control, RGZ- and RGZ and ZnPP-IX ( a HO-1 antagonist) combination-intervened groups (n=8), and the cell viability was detected by methyl thiazolyl tetrazolium (MTT) and the cell apoptosis was detected by flow cytometry. The cell PPARγ and HO-1 mRNA levels were detected by Real-time PCR, and the cell fibrosis-related protein expressions were detected by Western blot. Results The proliferation activity (A value) of HSC-T6 cells in RGZ-intervened group was (0.6±0.1), 38.4% decreased compared with (1.0±0.1) in the control (P<0.05), while it was (0.8±0.1) in RGZ and ZnPP-IX combination-intervened group, 17.2% decreased compared with in control group (P<0.05), but significantly increased compared with RGZ-intervened group (P<0.05); the apoptosis rate in RGZ-intervened group significantly higher than that in the control group (P<0.05), and the apoptosis rate in RGZ and ZnPP-IX combination-intervened group was significantly lower than that in RGZ-treated group (P<0.05). Conclusion RGZ intervention could significantly inhibit the proliferation and promote apoptosis of HSC-T6 cells in vitro, which might be related to the down-regulation of PPARγ and HO-1 mRNA levels.

Key words: HSC-T6 cells, Rosiglitazone, Cell proliferation, Apoptosis, Peroxisome proliferator-activated receptor γ, Heme oxygenase 1, In vitro