Objective:

To explore the role of Apelin-13 in alleviating post-stroke depression via regulation of BDNF mediated phosphorylation of forkhead box O 3A protein (FOXO3A) in rodent model of ischemic stroke.

Background:

Post-stroke depression (PSD) is a common complication in patients. Studies suggest that patients developing depression is associated with low-level serum brain derived neurotrophic factor (BDNF) that may increase the susceptibility to develop PSD. Treatment of PSD utilizes conventional drugs that are used to treat non stroke related mood disorders. However, limited success of these drugs have led researchers to investigate novel therapeutic strategies that can treat PSD. Apelin-13 is an adipocytokine that has been reported to exhibit beneficial effects in stroke as well as depression. Therefore, the present study aims to explore the role of Apelin-13 in alleviating PSD via regulation of BDNF mediated phosphorylation of forkhead box O 3A protein (FOXO3A) in rodent model of ischemic stroke.

Design/Methods:

Apelin-13 was administered to male SD rats post stroke and acute depression was induced. Rats were evaluated for functional and motor outcome at 24 h of reperfusion. Brains were harvested for infarct size estimation, biochemical assays, comparative histology and molecular studies. 

Results:

Apelin-13 rendered neuroprotection in PSD rats and alleviated depressive like behavior. It reduced infarct size and improved functional, and behavioral outcome. Normalization of biochemical parameters were achieved in Apelin-13 treated group. Reduction of FOXO3A phosphorylation with relation to BDNF expression was evident by relevant protein expression studies.

Conclusions:

This study provides a preliminary evidence of the role of Apelin-13 in ameliorating PSD which can further provide a rationale to explore it as a treatment approach.