Mitochondrial apoptotic pathway is involved in apoptosis in hippocampus of post-traumatic stess disorder rats
10.3969/j.issn.0529-1356.2010.02.007
- VernacularTitle:线粒体凋亡路径参与创伤后应激障碍大鼠海马神经元凋亡的调控
- Author:
Xiaoming LI
;
Fang HAN
;
Yuxiu SHI
- Publication Type:Journal Article
- Keywords:
Post-traumatic stress disorder;
Caspase-9;
Caspase-3;
Cytochrome C;
Western blotting;
Immunohistochemistry;
Rat
- From:
Acta Anatomica Sinica
2010;41(2):201-205
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the expressions of Caspase-9,Caspase-3, cytochrome C and their relationships, and investigate apoptotic mechanisms in hippocampus of post-traumatic stress disorder(PTSD) rats. Methods Sixty male Wistar rats were used in the present study. The single-prolonged stress (SPS)-method was used to set up the rat PTSD models. There were six groups:after SPS 1 day,4 days,7 days,14 days,28 days groups and control group. The expressions of caspase-9, Caspase-3 and Cytochrome C proteins were detected with immunohistochemistry, immunofluorescence and Western blotting. Results Immunohistochemical and immunofluorescent results showed that the expression of cytochrome C peaked at 4 days and maintained higher level at 7days after SPS. Expressions of Caspase-9 and Caspase-3 were increased and peaked at 7days after SPS. Western blotting results showed that compared with control group, cytochrome C protein was up-regulated and peaked at 4 days after SPS in the cytosol. Compared with the control group, cytochrome C tended to decrease in mitochondrial fractions. The activated form of Caspase-9 and caspase-3 were not detected in control group. They were present in model groups. Cleaved- caspase-9 and cleaved-caspase-3 peaked at 7 days after SPS, and then gradually decreased at 14 days. Conclusion The neuronal apoptosis in hippocampus of PTSD rats may be one of the causes inducing hippocampus atrophy. Mitochondrial apoptotic pathway is involved in apoptosis in the hippocampus of PTSD rats.
