Published online Aug 14, 2005. doi: 10.3748/wjg.v11.i30.4735
Revised: June 23, 2004
Accepted: June 24, 2004
Published online: August 14, 2005
AIM: To study the effect of rosiglitazone, which is a ligand of peroxisome proliferator-activated receptor gamma (PPARγ), on the expression of PPARγ in hepatic stellate cells (HSCs) and on the biological characteristics of HSCs.
METHODS: The activated HSCs were divided into three groups: control group, 3 µmol/L rosiglitazone group, and 10 µmol/L rosiglitazone group. The expression of PPARγ, α-smooth muscle actin (α-SMA), and type I and III collagen was detected by RT-PCR, Western blot and immunocytochemical staining, respectively. Cell proliferation was determined with methylthiazolyltetrazolium (MTT) colorimetric assay. Cell apoptosis was demonstrated with flow cytometry.
RESULTS: The expression of PPARγ at mRNA and protein level markedly increased in HSCs of 10 µmol/L rosiglitazone group (t value was 10.870 and 4.627 respectively, P < 0.01 in both). The proliferation of HSCs in 10 µmol/L rosiglitazone group decreased significantly (t = 5.542, P < 0.01), α-SMA expression level and type I collagen synthesis ability were also reduced vs controls (t value = 10.256 and 14.627 respectively, P < 0.01 in both). The apoptotic rate of HSCs significantly increased in 10 µmol/L rosiglitazone group vs control (χ2 = 16.682, P < 0.01).
CONCLUSION: By increasing expression of PPARγ in activated HSCs, rosiglitazone, an agonist of PPARγ, decreases α-SMA expression and type I collagen synthesis, inhibits cell proliferation, and induces cell apoptosis.