Captopril reverses chronic unpredictable mild stress-induced depression-like behavior in rats via bradykinin-B2r signaling pathway

Abstract

Purpose: To investigate the effect of captopril on chronic unpredictable mild stress (CUMS)-induced depression-like behavior in mice, and the involvement of the bradykinin-B2r signaling pathway in the process. Methods: Sixty healthy male C57BL/6J mice were assigned to control, model and high-, medium- and low-dose captopril groups and given the drug at doses of 9, 18 and 36 mg/kg, respectively. Open field and elevated cross maze tests were carried out, and escape latency in Morris water maze test was also test. The expressions of bradykinin B2R signal pathway proteins were assayed. Results: Open arm residence time and open arm entry times were significantly higher in captopril-exposed mice than in model mice, while 5-day escape latency values were significantly less in captopril-treated mice than in model group (p < 0.05). Protein expressions of B2R, bpnf and Cdc42 in captopril groups were significantly higher than those in model group (p < 0.05). Conclusion: Captopril mitigates CUMS-mediated depression-like disease in mice by regulating bradykinin B2R signal pathway. Therefore, captopril may play an antidepressant role by activating the expressions of B2R, bpnf and Cdc42.