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Original Research Article | OPEN ACCESS

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

Shaofeng Zhang , Lin He

Department of Psychiatry, Tianjin Anding Psychiatric Hospital, Tianjin 300000, China;

For correspondence:-  Shaofeng Zhang   Email: zshaofeng0610@163.com

Accepted: 27 September 2022        Published: 28 October 2022

Citation: Zhang S, He L. Captopril reverses chronic unpredictable mild stress-induced depression-like behavior in rats via bradykinin-B2r signaling pathway. Trop J Pharm Res 2022; 21(10):2131-2137 doi: 10.4314/tjpr.v21i10.13

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: Captopril, Bradykinin-B2r, Chronic unpredictable mild stress, Depression

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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