Objective:To investigate the effects of TGF-?1 on promoter activity of human transforming growth factor-beta1(TGF-?1) gene.Methods:The fragments with different length of the 5′-end sequence of the human TGF-?1 gene between -1 328 bp to +812 bp were obtained from a healthy male person genomic DNA, and the sequences were fused to chloramphenicol acetyltransferase reporter gene in the pCAT-enhancer plasmid to construct five chimeric recombinant plasmids. These recombinant plasmids were transiently transfected into rat hepatic setellate cell line(nFSC) by FuGENE6 transfection methods. The cells transfected with chimeric recombinant plasmids were cultured on media in the absence or presence of TGF-?1(2 5 ng/ml),CAT activities in transfected cells were tested and compared.Results:The different concentration of TGF-?1 can prevent the proliferation of nFSC, and these effects are dose-dependent; The presence TGF-?1 can stimulate the CAT activity of cells transfected with phTGF0 585?phTGF1 120?phTGF1 423?phTGF1 680?phTGF2 140 up to 2～5 times higher then cells cultured with absence of TGF-?1.Conclusion:The TGF-?1 can stimulate CAT activities in nFSC transfected with phTGF0 585?phTGF1 120?phTGF1 423?phTGF1 680?phTGF2 140. These results suggest that TGF-?1 have an autoregulation effect on TGF-?1 gene.

Objective To compare the different response of dermal fibroblasts from normal and scar-ring skin to cytokines,extracellular matrix and collagen promoter.Methods Human dermal fibroblast cul-ture was established by explanting tissue specimens from normal and scarring skin.Cellular proliferative ac-tivities were determined with BrdU-ELISA after treatment with IFN-?A,hIFN-?,TNF?and laminin for24hours.Reporter genes driven by collagen promoters were analyzed in two types of dermal fibroblasts trans-fected with consensus constructs48hours later.Results Dermal fibroblasts from normal and scarring skins showed different proliferative responses to IFN-?A,hIFN-?,TNF?and laminin,with stimulatory effects pre-sented in normal fibroblasts treated with IFN-?A,hIFN-?,TNF?and laminin,inhibitory effects presented in scarring fibroblasts treated with IFN-?A and laminin,and reduced or resistant effects presented in scar-ring fibroblasts to hIFN-?and TNF?.The5'flanking sequences(-2483~+42bp,-1448~+42bp)from human?1(Ⅰ)procollagen gene had lower activity of promoter in scarring fibroblasts compared with that in normal fibroblasts.Conclusion Compared with normal dermal fibroblasts,scarring dermal fibroblasts have reduced response or are resistant to some cytokines.Lower collagen production capacity is anticipated since collagen promoter activity is low in scarring dermal fibroblasts.The pathological mechanism of scarring for-mation might be related to the change of responses of dermal fibroblasts.

Objective to provide the evidence for inducing the SAP model in rats with proper concentration of sodium taurocholate.Methods 60 SD rats were divided into sham operated group, group of 1.5% in concentration, group of 3.5% in concentration and group of 5% in concentration randomly, while the SAP model was induced by the sodium taurocholate concentration of 1.5%,3.5% and 5% with the method of retrograde injection into the biliopancreatic duct.To calculate the mortality of different groups, measure the serum amylase, tumor necrosis factor -α(TNF -α) and interleukin -6 (IL -6),and to observe the pancreatic pathological scores of HE staining in rats.Results The mortality in group of 5% in concentration has a significant ascending compared with group of 1.5% in concentration, while the serum amylase, tumor necrosis factor -α(TNF -α) , interleukin -6( IL -6), pathological score of hemorrhage and acinar necrosis in group of 5% in concentration have a significant ascending compared with group of 1.5% in concentration and group of 3.5% in concentration.Conclusions A better SAP model may be induced by sodium taurocholate with the concentration of 5% by the method of retrograde injection into the biliopancreatic duct, which may accord with the physiological and pathological manifestation of SAP.

Objective To explore the effect of atorvastatin on the proliferation and apoptosis of K562 cells andto investigate its mechanisms.Methods The cells were treated by different concentrations of atorvastatin.The CCK-8 assay was employed to detect the cell proliferation.The cell apoptosis was detected by AnnexinV-FITC/PI dual staining;the flow cytometry was used to detect the cellular cycle;the activities of caspase-3,-8,-9 were detected by the colorimetric method;qRT-PCR was employed to measure the mRNA expression levels of Bcl-2 and PDCD5 in K562 cells.Results Atorvastatin could inhibit the proliferation of K562 cells in a time-and dose-dependent manner(P＜0.05);and induced the apoptosis of K562 cells,the percentage of G0/G1 phase cells was increased after atorvastatin treating k562 cells(P＜0.01),while the percentage of S phase cells was decreased(P＜0.01),moreover which showing the concentration dependence(P＜0.01);atorvastatin activated the caspase-3,-8,-9 (P＜0.01);down-regulated Bcl-2 mRNA expression and up-regulated PDCD5 mRNA expressionin a concentration dependence(P＜0.01).Conclusion Atorvastatin can inhibit the proliferation and induce apoptosis in K562 cells.