Objective To investigate the protective effect and it's possible mechanism of Tanshinone ⅡA in radiation-induced pulmonary fibrosis.Methods Having the right hemithorax of female Wistar rats irradiated(30?Gy) in 10 fractions within 14 days by 6 ?MV photons,the radiation-induced pulmonary fibrosis animal model was established.In the treatment group,sodium Tanshinone ⅡA sulfonate(15?mg/kg) was given by intraperitoneal injection 1 hour before each fraction of irradiation.Five months after irradiation,the difference of the histopathological changes,the hydroxyproline content and expression of TGF-?1 between the radiation alone group,tanshinone plus radiation and control group were analyzed by HE stain,Massion stain,immunohistochemical methor and reverse transcriptase polymerase chain reaction(RT-PCR) method.Results The histopathological comparison revealed the protective effect of Tanshinone ⅡA.The content of hydroxyproline was(21.99?3.96),((38.25?)(7.18)),(28.94?4.29)??g/g in the control group,radiation alone group and radiation plus Tanshinone ⅡA.The expression of TGF-?1(mRNA and protein) was reduced by Tanshinone ⅡA.Pathological changes of the pulmonary fibrosis was reduced by Tanshinone ⅡA yet.Conclusions Our study shows that Tanshinone ⅡA can inhibit radiation-induced pulmonary fibrosis,and the possible mechanism of its may be made possible through down-regulating the expression of TGF-?1 in the irritated lung tissue.

Objective To investigate the relationship of ELK-3 and epithelial-mesenchymal transition ( EMT) for ex-ploring its possible mechanism .Methods The human hepatocellular carcinoma cells ( HCC) were divided into small interference RNA transfection group and Ras-ELK-3 pathway inhibitor group .The protein level of ELK-3 target gene EGR-1 E-cadherin ,vimentin and p38 in HCC were determined by Western blot analysis .Results The protein level of ELK-3 and its target gene EGR-1 in treated human hepatocellular carcinoma cells significantly decreased as compared with the negative control group (P<0.01).The protein level of E-cadherin was significantly increased (P<0.01), while vimentin and p38 were decreased in HCC cells with ELK-3 interference (P<0.01).Conclusions ELK-3 in-terference can inhibit the epithelial-mesenchymal transition of HCC cells by down-regulating p38.