ABSTRACT
Purpose To investigate the expression and clinical significance of Foxp3 ( cell surface marker of regulatroy T) mRNA and its protein in endometrial carcinomas and normal endometrial tissues. Methods Real-time fluorescence quantitative PCR and immuno-histochemical SP methods were used to detect the expressions of mRNA and protein in tumor tissue of 84 cases of endometrial carcino-mas and 40 cases of normal endometrial tissue, then to analyze the relationship between Foxp3 gene and clinical pathological character-istics of endometrial carcinoma specimens, such as differentiation, FIGO stage. Results Foxp3 mRNA and it′s protein expression of endometrial carcinomas were significantly higher than that of normal endometrial tissues. There were significantly relationships between Foxp3 mRNA expression and FIGO stage of endometrial cancer, Foxp3 mRNA expressions of III+IV stage was higher than that ofⅠ+Ⅱ stage endometrial carcinoma (P<0. 05). But the relationship between Foxp3 expression and differentiation degree reached differ-ent conclusions in the two detection methods. By immunohistochemistry the expression of Foxp3 protein was correlation with histological differentiation grade (rs =0. 72, P <0. 01). In poorly differentiated endometrial carcinoma Foxp3 + cell number was significantly higher than that in well differentiated endometrial carcinoma. By detection of real-time fluorescence quantitative PCR method, Foxp3 mRNA expression was not correlated with tumor grade (rs =0. 01, P=0. 35). Conclusion Foxp3 in endometrial carcinomas are high expressions. Immunohistochemical method has more clinical value than real-time fluorescence quantitative PCR test results. Foxp3 may be involved in the regulation of the development of endometrial cancers.
ABSTRACT
BACKGROUND: Cerebrovascular disease often causes dysfunction of the brain nerve, and nerve cel apoptosis is the important factor of cerebral nerve dysfunction. The excessive expression of c-fos can block the transduction of intracelular signal so that producing some apoptosis-promoting factors, which involve in nerve cel apoptosis process after ischemia injury of brain. Bcl-2 is an inhibited factor. It might to be the key to treat ischemic cerebrovascular disease by inhibiting or reducing the apoptosis of nerve cels after ischemia injury. OBJECTIVE: To investigate the therapeutic effect and mechanism of the Total Flavone of Hawthorn Leaf on chronic cerebral ischemia rats. METHODS: A total of 72 healthy male Sprague-Dawley rats were randomly divided into sham surgery group, model group, Total Flavone of Hawthorn Leaf group and ginkgo leaf group. Permanent bilateral carotid artery ligation was used to prepare chronic cerebral ischemia model in the model group, Total Flavone of Hawthorn Leaf group and ginkgo leaf group. Total Flavone of Hawthorn Leaf group and ginkgo leaf group respectively received 140 mg/kg Total Flavone of Hawthorn Leaf and 12.3 mg/kg ginkgo leaf intragastricaly for 36 days from 36 days after model induction. Model group and sham surgery group received 3.5 mL/kg physiological saline intragastricaly. RESULTS AND CONCLUSION: Compared with the model group, the expression of c-fos protein significantly deceased in the Total Flavone of Hawthorn Leaf group (P 0.05). These data indicated that the protective effect of Total Flavone of Hawthorn Leaf on chronic cerebral ischemia was associated with its inhibition of neuronal apoptosis. Its mechanism of anti-apoptosis might be associated with up-regulating expression of Bcl-2, down-regulating expression of c-fos and decreasing Ca2+ content in brain.