Objective To explore the possible anti-inflammatory mechanism of peroxisome proliferators-activated receptor（PPAR） gamma-agonists by investigating the effects of Rosiglitazone on the expression of phosphorylation of signal transducer and activator of transcription 6（p-STAT6） and the secretion of interleukin（IL）-4 in T-lymphocytes from patients with acute asthma.Methods Peripheral blood T-lymphocytes from 10 healthy volunteers（group A） and 10 patients with acute asthma were isolated，purificated and cultured.T-lymphocytes from the asthma patients were divided into a control group（group B） and a Rosiglitazone treated group（group C）.Rosiglitazone was added with a single dose of 10-4 mol/L at 0 hour of cultrue.After cultured for 48 hours，the concentration of IL-4 in supernatant of each groups were detected by ELISA.The express of p-STAT6 in the T-lymphocytes were determined by Western blot and immunohistochemical techniques.Results The levels of IL-4 were increased markedly in group B than those in group A and group C[（170.34±9.05）pg/mL vs（76.82±7.06）pg/mL and（123.59±8.70）pg/mL，both Plt;0.01]，and which in group C was significantly lower than group A（Plt;0.01）.The levels of p-STAT6 in T lymphocytes were increased markedly in group B than in group A and C[Western blot：（6.28±0.19 vs 3.07±0.18 and 4.12±0.16；immunohistochemistry：（36.58%±7.41）% vs（11.39±4.02）% and（23.92±5.8）%，all Plt;0.01），and which in group C were significantly higher than that in group B（both Plt;0.01）.There was a positive correlation between the level of p-STAT6 and IL-4（Plt;0.01）.Conclusion The levels of p-STAT6 and IL-4 in T-lymphocytes of patients with acute asthma were suppressed by Rosiglitazone in vitro.
Objective To study the effects of peroxisome proliferators-activated receptor (PPAR) γ on the growth of human hepatocellular carcinoma cells and explore the roles of phosphatase and tensin homologue deleted on chromosome ten (PTEN) and phospho-Akt in this process. Methods SMMC-7721 cells were treated with 15-d-PGJ2 or pioglitazone, which were two kinds of PPARγ ligands, at different concentrations. The viability of SMMC-7721 cells was evaluated by MTT assay. The cell cycle was analyzed by flow cytometry. PTEN mRNA level was determined by RT-PCR. The protein expressions of PTEN and pAkt were measured by Western blot analysis. Results It was demonstrated through MTT assay that both 15-d-PGJ2 and pioglitazone had an inhibitory effect on the growth of SMMC-7721 cells in a time- and dose- dependent manner. According to flow cytometry detection, more cells were arrested in G0/G1 phase. Increased expression of PTEN mRNA was detected in 15-d-PGJ2 or pioglitazone-treated cells through RT-PCR. Increased expression of PTEN protein and decreased expression of pAkt were confirmed by Western blot analysis. Conclusion The ligands of PPARγ could inhibit SMMC-7721 cells proliferation in a time- and dose- dependent manner. The upregulation of PTEN may be involved in the underlying mechanism.