Fluoxetine protects against inflammation and promotes autophagy in mice model of post-traumatic stress disorder.

Post-traumatic stress disorder is a major public health problem due to its frequency, chronicity, and disability that impact daily life. Studies have evidenced that the activation/inhibition of autophagy and excessive activation of microglia have a relationship with PTSD. For this purpose, C57BL/6 mice were employed to establish the post-traumatic stress disorder pathology mice model by conditioned fear and single prolonged stress (CF + SPS). Fluoxetine and PLX3397 were administered. PTSD-like behaviors were alleviated following fluoxetine treatment, evidenced via open field and conditioned fear test. Autophagy-associated proteins were upregulated, and inflammation factors were reduced after fluoxetine treatment. Microglia depletion mice showed a lower inflammatory level. In conclusion, fluoxetine can promote autophagy and inhibit neuroinflammation in mice model of PTSD, providing a theoretical basis for fluoxetine in treating PTSD.