Effect of cyclooxygenase‑2 inhibition on the development of post‑traumatic stress disorder in rats

Post‑traumatic stress disorder (PTSD) is characterized by re‑experiencing of a traumatic event, avoidance of trauma‑associated stimulation, general changes in mood and cognition, and hyper arousal symptoms. Cyclooxygenase is involved in the production of prostaglandins and thromboxanes, and its inducible form cyclooxygenase‑2(COX‑2), an important mediator of cell injury in inflammation, is primarily expressed in leukocytes and brain cells. The present study investigated the expression of COX‑2 in the hippocampi of rats with PTSD and evaluated the effect of COX‑2 inhibition on PTSD. Adult male Wistar rats were randomly divided into three groups: Control (n=20), PTSD (n=20) and intervention group (PTSD+COX‑2 inhibitor treatment, n=20). The expression of COX‑2 was detected by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling staining was used to observe the apoptosis of rat hippocampal neurons. Tumor necrosis factor α (TNF‑α), interleukin (IL)‑6 and prostaglandin E2 (PGE2) levels were analyzed by ELISA. Nitric oxide (NO) was detected using the Griess test. The behavioral and cognitive function of rats in the PTSD group was significantly decreased compared with the control group, while the behavioral and cognitive function of rats in the intervention group were improved. The COX‑2 mRNA and protein expression levels in hippocampi of rats in the PTSD group were higher than in the control and intervention group. The apoptosis of hippocampus in rats with PTSD was significantly increased compared with the control group and following treatment with COX‑2 inhibitor, apoptosis was decreased. In addition, compared with the control group and intervention group, the levels of TNF‑α, IL‑6, PGE2 and NO in hippocampi of rats were increased in the PTSD group. The present study indicated that COX‑2 may be involved in the pathogenesis of PTSD, and inhibition of its expression serves a neuroprotective role in hippocampi of PTSD rats.