Abstract

In this study, sinapic acid was evaluated for its effect on depressive behavior of normal mice and stressed mice. Swiss albino male mice were given unpredictable mild stressors for twenty-one consecutive days to produce depressive behavior. Sinapic acid (5, 10, 20 mg/kg) and fluoxetine (20 mg/kg) were given orally to mice for twenty-one days in succession. Depressive behavior was detected by tail suspension test and sucrose preference test. After behavioral testing, biochemical estimations were performed in plasma (nitrite, corticosterone) and brain (MAO-A, malondialdehyde, reduced glutathione, catalase, TNF-α). Histopathological studies on the brain were also performed. The immobility time of mice in the tail suspension test was remarkably decreased by sinapic acid (5 and 10 mg/kg). Sinapic acid restored the decreased sucrose preference in mice exposed to the stress paradigm. It also remarkably lowered concentration of plasma nitrite and corticosterone; brain malondialdehyde, monoamine oxidase- A and TNF-α; and increased the concentration of brain catalase and GSH in normal mice and also stressed mice. Histopathological studies indicated protective effect of sinapic acid against hyperchromatic nuclei in the brain. Thus, sinapic acid produced remarkable antidepressant effect in normal mice and also stressed mice. The possible mechanisms for the observed antidepressant effect of sinapic acid might be through inhibition of brain MAO-A, amelioration of neuroinflammation and oxidative stress; decrease of plasma corticosterone and protection against hyperchromatic nuclei in the brain.

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