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Understanding the mechanism by which FA ameliorates depression and pain as a multi-targeted compound could open new avenues for the development of innovative treatments for depression coupled with pain.Īdell A (2004) Antidepressant properties of substance P antagonists: relationship to monoaminergic mechanisms? Curr Drug Targets CNS Neurol Disord 3:113–121Īrora V, Kuhad A, Tiwari V, Chopra K (2011) Curcumin ameliorates reserpine-induced pain-depression dyad: behavioral, biochemical, neurochemical and molecular evidences.
The findings suggest that FA exerts the effects on reserpine-induced pain and depression-like behaviors through regulating monoaminergic system, oxidative/antioxidant defense, inflammatory and apoptotic signaling pathways. Furthermore, FA produced a dose dependent decrease in substance P, NF-κβ p65 and caspase-3 levels in the frontal cortex and hippocampus of reserpinised mice. The higher dose of FA effectively antagonized the oxidative and nitrosative stress and inflammation as evidenced by down-regulated nitrite, LPO, IL-1β, TNF-α, and up-regulated GSH and SOD.
Treatment with FA (40 or 80 mg/kg, p.o.) reversed the behavioral abnormalities and decreased norepinephrine, serotonin and dopamine levels in the hippocampus and frontal cortex induced by reserpine. The neurochemical assays suggested the decreased neurotransmitters (dopamine, norepinephrine and serotonin) along with the increased oxidative stress, inflammatory cytokines, and apoptotic parameters in the frontal cortex and hippocampus of the reserpinised mice. The results showed that reserpine (1 mg/kg for 3 days, i.p.) led to a significant decrease in nociceptive threshold in thermal hyperalgesia and mechanical allodynia, as well as a significant increase in the immobility time in mouse models of despair test. The present study aimed to investigate the effect of ferulic acid (FA) on reserpine-induced pain and depression-like behaviors in mice. Depression and pain influence each other, but the mechanisms are still obscure.
#FA TRESHHOLD IN MEDINRIA FOR MOUSE BRAIN SERIES#
Depression-pain dyad involves a series of pathological changes including the dysfunction of neuroendocrine and immune networks.
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