Effects of Sodium Ferulate on Cognitive Function in Hippocampus of Chronic Cerebral Hypoperfusion Rats

Objective: To assess sodium ferulate's effect on cognitive function and p38MAPK signaling in hippocampus of rats with chronic cerebral hypoperfusion (CCH). Methods: 45 male Sprague-Dawley (SD) rats were separated into sham-operation group, CCH model group and treatment group (intraperitoneal injection of 50 mg/kg sodium ferulate). The cognitive function was detected via open-field test, novel object recognition test and Morris water maze test. The activity of superoxide dismutase (SOD) in hippocampal tissues was detected using ELISA kit. Moreover, the neuronal damage in hippocampal tissues was assessed by immunohistochemical method, and apoptosis was assessed via TUNEL staining. Finally, p-p38MAPK signaling protein level in hippocampal tissues was detected via Western blotting. Results: No difference was found in rat autonomic activity among three groups (P > 0.05). The novel object recognition ability of model rats was significantly impaired along with longer escape latency and shorter retention time in the target quadrant (P < 0.01), which were all improved after sodium ferulate treatment (P < 0.01). SOD activity in hippocampal tissues in model rats was significantly reduced and sodium ferulate could significantly increase SOD activity (P < 0.01). There were a large number of damaged neurons and apoptotic cells in hippocampal tissues in model group and sodium ferulate could protect neurons (P < 0.01). The levels of p-p38MAPK, GSP3 beta and p-tau protein in hippocampal tissues in model group were significantly increased, which were significantly reduced after treatment with sodium ferulate (P < 0.01). Conclusion: Sodium ferulate can protect the CCH-induced cognitive impairment in rats and reduce the CCH-induced damage and apoptosis of hippocampal neurons, possibly through inhibition of p38MAPK signaling pathway.