p-Coumaric acid mitigates lipopolysaccharide induced brain damage via alleviating oxidative stress, inflammation and apoptosis.

OBJECTIVES

Systemic administration of lipopolysaccharide induces neuroinflammation leading to cognitive deficit and memory impairment. Herein, we investigated the effects of p-Coumaric acid (PCA) in LPS induced neuroinflammation in mice. PCA is reported to possess free radicle scavenging and neuroprotective action.

METHODS

Mice received treatment with PCA (80 mg/kg, and 100 mg/kg, p.o.) for 28 days. LPS (0.25 mg/kg) was administered intraperitoneally from Day 15 to 21, to all groups. Memory impairment and cognitive deficit were assessed by MWM and Y maze test, followed by estimation of ROS, TNF-α, IL-6, caspase-3 and c-Jun in the brain homogenate by ELISA. Histopathological changes were investigated using Nissl and H&E staining.

KEY FINDINGS: PCA attenuated increased oxidative stress, significantly increasing SOD, GSH levels and decreasing MDA level and AChE activity in mice brain, lowered the levels of TNF-α and IL-6 indicating protection against neuroinflammatory reaction. PCA also suppressed neuronal apoptosis, as indicated by decreased levels of caspase-3 and c-Jun. Further, histopathological findings revealed that PCA attenuated neuronal loss and pathological abnormalities in the hippocampus.

CONCLUSIONS

Our findings give compulsive evidence suggesting a protective effect of PCA in neuroinflammation, cognitive impairment and neuronal apoptosis induced by LPS, through its antioxidant, AChE inhibitory, anti-inflammatory and antiapoptotic activity determined by behavioural, biochemical and histopathological measures.