[The effect or rosiglitazone on signal pathways of transforming growth factor-beta1 in human lung fibroblast].

OBJECTIVE: To investigate the expression of CTGF, CTGF mRNA, NF-kappaB and AP-1 induced by TGF-beta1 in human lung fibroblast (HLF-02), and study the effect and possible mechanism of rosiglitazone on signal pathways of TGF-beta1 in HLF-02. METHODS: The effects of TGF-beta1, curcumin, PDTC and rosiglitazone on the expression of CTGF, NF-kappaB and AP-1 were evaluated with Western blot. The expression of CTGF was also detected with immunohistochemistry assay. The level of CTGF mRNA was detected with RT-PCR. RESULTS: (1) The CTGF protein levels of HLF-02 cells were significantly up-regulated after incubated with 1 ng/mL TGF-beta1 for 15 min (P<0.01 vs Control). The CTGF mRNA was also up-regulated. The levels of CTGF protein and CTGF mRNA expression was up-regulated by TGF-beta1 in a time-dependent manner. (2) The expression of NF-kappaB and AP-1 increased after HLF-02 cells were incubated with 1 ng/mL TGF-beta1 for 30 min (P<0.01 vs Control). The CTGF protein levels were inhibited obviously after HLF-02 cells were incubated with PDTC or curcumin. (3) The expression of CTGF, NF-kappaB and AP-1 decreased after pre-incubation with different doses of rosiglitazone (P<0.01 vs TGF-beta1 group). The CTGF mRNA were also markedly inhibited (P<0.01 vs TGF-beta1 group). CONCLUSION: It is supposed that rosiglitazone inhibits CTGF expression induced by TGF-beta1 in HLF-02 cells by activating PPARgamma through NF-kappaB and AP-1 signal transduction pathways.