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.
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.