Betanin, in conjunction with virgin coconut oil, suppresses lipopolysaccharide-induced neuroinflammation in C57BL mice by modulating the NLRP3 inflammasome pathway

BACKGROUND: The third basic pathology of Alzheimer’s disease (AD) has been recognized as the occurrence of neuroinflammation in the brain. Microglial-mediated neuroinflammation and neurodegenerative disorders are both closely related to NLRP3 inflammasome activation.METHODS: We investigated the effect of BET along with VCO in LPS-induced cognitive deficit in C57BL mice using behavior tests, measuring oxidative stress, and quantitative estimation of NLRP3, IL-1β.RESULTS: LPS exposure produces cognitive impairment in mice via NLRP3 activation, as measured by the Morris water maze and elevated plus maze tests. When administered orally, betanin and virgin coconut oil (BET 200 mg/kg + VCO 2 g/kg and BET 400 mg/kg + VCO 10 g) reversed memory loss by restoring abnormal NLRP3 (F(8, 45)=5.571, P<0.0001) and IL-1β (F(8, 45)=4, P=0.0004), and the acetylcholinesterase level (F(8, 45)=3.487, P=0.0033) in the brain. We observed that there was an increase in the levels of antioxidant enzymes such SOD (F(8, 45)=7.644, P<0.0001), CAT (F(8, 45)=2.510, P=0.0239), GSH (F(8, 43)=10.87, P<0.0001), and a decline in the levels of MDA (F(8, 45)=4, P=0.0006). According to the results of H and E staining, early neuronal inflammation and necrosis in the cortex and hippocampus of the mice were significantly reduced with the combination treatment.CONCLUSIONS: The current study indicated that combining was more effective than either BET or VCO alone and could be a safe, cost-effective, and multi-target therapeutic approach.