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.
ABSTRACT
Background and purpose:Esophageal cancer is a serious disease threatening human health, and it is very difficult to understand the development mechanism and find the therapeutic methods for esophageal cancer. In recent years, B7-H3, as a new member of B7 immunoregulatory superfamily, overexpressed in multiple tumor types, is considered to be a new tumor marker and potential therapeutic target. This study aimed to detect the expression of B7-H3 in esophageal cancer cell lines TE-1, TE-13, Eca-109 and exploring the effect of B7-H3 siRNA on cell proliferation, migration and invasionin vitro in human esophageal cancer Eca-109 cell line. Methods:The expression of B7-H3 in esophageal cancer cell lines TE-1, TE-13 and Eca-109 were detected by reverse transcription polymerase chain reaction (RT-PCR). B7-H3 siRNA and control siRNA were transfectedin vitro into human esophageal cancer Eca-109 cells using LipofectamineTM 2000. The expressions of B7-H3 mRNA and protein in Eca-109 cells were analyzed by RT-PCR and Western blot. The proliferation, migration and invasion abilities of Eca-109 cells were measured by MTT assay, wound scrape assay and transwell invasion assayin vitro,respectively.Results:All tested cultured esophageal cancer cell lines constitutively expressed B7-H3 mRNA under normal conditions (TE-1 0.382±0.008, TE-13 0.399±0.008, Eca-109 0.428±0.012). After transfection, the expression of B7-H3 mRNA levels decreased in B7-H3 siRNA transfected group, compared with control siRNA transfected group (0.128 5±0.000 2vs 0.532 4±0.000 7,P0.05).Conclusion:All tested esophageal cancer cell lines constitutively express B7-H3 mRNA. B7-H3 siRNA interference inhibits Eca-109 cell migration and invasion abilities. B7-H3 may have a critical role in regulating Eca-109 cell progression.