The role and mechanism of gastrodin in the medial prefrontal cortex autophagy of PTSD rats.

BACKGROUND

This study provided a reliable experimental basis for exploring the pathogenesis of PTSD-induced memory impairment, fear abnormalities, and affective disorders, aiming to facilitate new thinking for the prevention, treatment, and drug development of clinical PTSD.

MATERIAL AND METHODS

A rat model of PTSD was established by continuous single stress stimulation method. The Morris water maze was used to detect the learning and spatial memory exploration abilities of rats. The autonomic motion behavior, fear, and anxiety of rats in each group was detected by the elevated plus maze test and the open field test. The immunofluorescence method was employed to observe and detect the changes of autophagy in mPFC neurons of PTSD rats. Western blotting was used to detect the expressions of autophagy-related genes Beclin-1 and LC3, autophagy substrate p62 protein, and apoptosis-related factors Bcl-2 and Bax.

RESULT

Gastrodin could improve the learning and spatial memory abilities of PTSD-SPS rats, the reduction of active movement and inquiry behavior, and the autophagy of mPFC neurons, and also increase the expressions of Beclin-1, LC3-I, LC3-II, and Bax proteins, as well as decrease the expressions of Bcl-2 and p62.

CONCLUSIONS

Gastrodin is effective in the treatment of PTSD-induced memory impairment, fear abnormalities, and affective disorders. The mechanism is related to autophagy in mPFC neurons.