Background: Post-traumatic stress disorder (PTSD) is a stress-related psychosomatic disorder caused by occurrence of a traumatic event and the hippocampus volume of the patients with Post-traumatic stress disorder decreased.However, the mechanisms Feminine Medicated Products that cause such damage are not well-understood.The aim of this study is to detect the expression of apoptosis-related Bax, Bcl-2, Caspase-3 and Insulin-like growth Factor-I proteins in the hippocampus region in the Predatory stress rats.Materials and Methods: A total of 70 male wistar rats were divided into Predatory stress groups of 1d, 2d, 3d, 7d, 14d, 30d and a normal control group (N = 10).
Rats were subjected to 5 min of predatory stress and then exposed to the elevated plus-maze (EPM).Serum corticosterone and Insulin-like growth factor-1 level of Hippocampus were measured by ELISA technique.The expression of Bax, Bcl-2, and Caspase-3 were detected by western blotting.Results: Rats spent significantly more time in closed arms of the elevated plus maze (EPM) than control group after exposure to stress.
Serum levels of corticosterone significantly increased at 2d-3d.The expression of hippocampal IGF-1 was significantly up-regulated at 1d-2d after stress.Both Bax and the ratio of Bax/Bcl-2 significantly peaked at Predatory stress 2d-14d.Caspase3 was significantly active among 2d-30 compared to the normal control.
Conclusion: The activation of caspase-3 in the stress groups indicates that apoptosis may be one of the reasons inducing hippocampus atrophy and play roles in the pathogenesis of PTSD.Increase in hippocampus levels of IGF-1 during early Engraved 40oz Tumbler PTSD might be involved in the early molecular inhibitory mechanism of apoptosis in PTSD.