INTRODUCTION: Present investigation determines the beneficial effect of picroliv against lipopolysaccharide (LPS)-induced neuronal inflammation and injury. MATERIAL AND METHODS: Neuronal injury was induced by LPS 250 µg/kg, i.p. for the period of one week, and picroliv 12.5 and 25 mg/kg was given i.p. 30 min prior to the administration of LPS for the duration of 12 days. The effect of picroliv was determined on the cognitive function by Morris water maze (MWM). Mediators of inflammation were estimated by using enzyme-linked immunosorbent assay (ELISA) and western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis was done to determine the expressions of several proteins. RESULTS: Data of the study reveal that picroliv ameliorates the reduced memory impairment and cognitive dysfunction in LPS-induced mice. Moreover, expressions of inflammatory protein and -amyloid protein and level of inflammatory mediators were found to be reduced in the picroliv-treated group as compared to the negative control group. Data of RT-PCR reveal that the gene of Toll-like receptor 4 (TLR-4), -synuclein, neurotrophic factor (BDNF) and interleukin-1 (IL-1) protein were also decreased in the picroliv-treated group as compared to the negative control group. In addition picroliv attenuates the altered level of nuclear factor-kB(p-NF-kB), amyloid- (A), -synuclein and glial fibrillary acidic protein (GFAP) positive cells in the brain of LPS-induced mice. CONCLUSIONS: The report concludes that picroliv protects the neuroinflammation and injury in LPS-induced mice by regulating the inflammatory pathway.
INTRODUCTION: Present investigation determines the beneficial effect of picroliv against lipopolysaccharide (LPS)-induced neuronal inflammation and injury. MATERIAL AND METHODS:Neuronal injury was induced by LPS 250 µg/kg, i.p. for the period of one week, and picroliv 12.5 and 25 mg/kg was given i.p. 30 min prior to the administration of LPS for the duration of 12 days. The effect of picroliv was determined on the cognitive function by Morris water maze (MWM). Mediators of inflammation were estimated by using enzyme-linked immunosorbent assay (ELISA) and western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis was done to determine the expressions of several proteins. RESULTS: Data of the study reveal that picroliv ameliorates the reduced memory impairment and cognitive dysfunction in LPS-induced mice. Moreover, expressions of inflammatory protein and -amyloid protein and level of inflammatory mediators were found to be reduced in the picroliv-treated group as compared to the negative control group. Data of RT-PCR reveal that the gene of Toll-like receptor 4 (TLR-4), -synuclein, neurotrophic factor (BDNF) and interleukin-1 (IL-1) protein were also decreased in the picroliv-treated group as compared to the negative control group. In addition picroliv attenuates the altered level of nuclear factor-kB(p-NF-kB), amyloid- (A), -synuclein and glial fibrillary acidic protein (GFAP) positive cells in the brain of LPS-induced mice. CONCLUSIONS: The report concludes that picroliv protects the neuroinflammation and injury in LPS-induced mice by regulating the inflammatory pathway.
Authors: Rajesh N Kalaria; Stephen B Wharton; Rachel Waller; Yoshiki Hase; Julie E Simpson; Paul R Heath; Matthew Wyles Journal: Transl Stroke Res Date: 2022-05-31 Impact factor: 6.800