Objective To analyze the effects of TGF-β1 and p53 on expressions and mutations in smoked lung tissues.Methods Smoked rats model was built.The expressions of TGF-β1 and p53 in lung tissues were observed by immunohistochemistry.The expressions of TGF-β1 mRNA in lung tissues were observed by trans-reverse polymerase chain reaction (RT-PCR).The mutations of p53 in exon 5,6,7-8 were analyzed by polymerase chain reaction single-strandconformational polymorphism (PCR-SSCP).Results The expressions of TGF-β1 in normal lung tissues were faint,and the expressions increased along with the smoking months (P ＜0.05).The positive ratio of protein expression was increased with prolonging smoking time.The mutation of p53 was increased with smoking time.The p53 exons 5,6,7-8 have mutations respectively.The ratio of mutations increased along with smoke months.Conclusion The expressions and mutations of TGF-β1 and p53 increase along with smoked time,which can be regarded as references for lung cancer diagnosis.

Objective To observe the influence of long-term smoking on the expression of p53 and K-ras in rat lung tissues, and to study the relationship of smoking to the mutation of p53 and K-ras gene. Methods The model of Wistar rat smoking was built up. Seventy-two healthy male Wistar rats were divided into the experimental group and control group at random. The rats of the experimental group were compelled to smoke, and the rats of the control group were given the same condition as the experimental group was, without smoking. The rats of the experimental group were smoked for 6 months. At the end of each month, 6 rats were chosen from the two groups respectively, their lung tissues were sampled and immunohistochemistry was applied to observe the expression of p53 and K-ras in lung tissues. Finally, the mutation which might happen in the exon 5, 6, 7-8 of p53 and the exon 1 of K-ras was examined by PCR-SSCP. Results The p53 protein was expressed in cell nucleus and K-ras in cytoplasm. The positive ratio of protein expression was increased with the extension of smoking time. The mutation of p53 was increased as the smoking time extended. But the effect of smoking time was not that significant on the mutation of K-ras.Conclusion Smoking can strengthen the expression of p53 and K-ras protein and can also result in gene mutation. As the time of smoking extended, those phenomenons were tending to rise. That provided the theoretical evidence which can be used to judge the lesion of lung tissues caused by smoking and help the early diagnosis of smoking-related lung carcinomas. It is of great theoretical and application values.

Objective To investigate the effect of expressions of P53 and VEGF in smoking lung cancer and surrounding lung tissue,and to offer us with theorial evidence of early diagnosing smoking-related lung carcinoma clinically.Methods126 lung cancer patients were recruited,including 96 long-term smoking and 30 nonsmoking patients.All clinical data was integrity and the patients had clear smoking history.None of patients underwent chemotherapy,radiotherapy and other tumor treatment.The bronchial epithelium,cancer tissues,pericancer lung tissues,surrounding lung tissues were observed by light microscopy,and the expressions of P53 and VEGF of lung cancer tissues,pericancer lung tissues and surrounding lung tissues were detected by Immunohistochemical methed in smoking and non-smoking group.The experimental data was analyzed by SAS statistical software and the degree of difference between the groups was compared accordingly.ResultsThere were different levels of expansion of alveolar wall in lung tissues of smokers,and alveolar wall became capsular to expand.Respiratory bronchioles were cystic expansion and small bronchial wall becomed thickening,with severe bronchial epithelial membrane ranking nuts-chaos and peeling.Goblet cells and the cell surface of the cavity mucous secretions and suppositories were more than those of non-smokers.The P53 protein was expressed in cell nucleus and VEGF expressed in the cytoplasm and endothelial cells of neovascularization.Both their positive behavior was granular brown.Either for smoking or for non-smoking lung cancer,the expressions of P53 and VEGF were higher in tumor tissues than that of in the pericancer and surrounding lung tissue(P