Neuroinflammation is a complicated process that involves the activation of the brain's innate immune system in response to various stressors such as infection, injury, and neurodegeneration.Present review mainly focused on the possible signaling pathways and future potential targets for Omeprazole(OM) in neuroinflammation to combat neurodegenerativediseases like Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), stroke, traumatic brain injury (TBI) and many more.OM dramatically reduced TNF-α, IL-1β, and IL-6 levels. It also reduces oxidative stress by increasing the activity of antioxidants such as SOD, catalase activity, and palliating pro-oxidant malondialdehyde (MDA).OM suppressed inflammatory biomarkers by interrupting the nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κβ) signaling pathway in gastrointestinal disorders and renal injury.Excessive NMDA receptor activation causes an influx of Ca2+ ions into the neuron, disrupting cellular homeostasis and produce reactive oxygen species. OM cause deregulation, and injured mitochondrial-mediated ROS generation. OM potently diminished the malondialdehyde level, serum IL-1β and sE-selectin,and caspase-3, and increased levels of glutathione, Bcl-2 by PPAR-γ, NF-κB, and Nrf2/HO-1 Signaling Pathways.

Neuroinflammation is a complicated process that involves the activation of the brain's innate immune system in response to various stressors such as infection, injury, and neurodegeneration.Present review mainly focused on the possible signaling pathways and future potential targets for Omeprazole(OM) in neuroinflammation to combat neurodegenerativediseases like Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), stroke, traumatic brain injury (TBI) and many more.OM dramatically reduced TNF-α, IL-1β, and IL-6 levels. It also reduces oxidative stress by increasing the activity of antioxidants such as SOD, catalase activity, and palliating pro-oxidant malondialdehyde (MDA).OM suppressed inflammatory biomarkers by interrupting the nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κβ) signaling pathway in gastrointestinal disorders and renal injury.Excessive NMDA receptor activation causes an influx of Ca2+ ions into the neuron, disrupting cellular homeostasis and produce reactive oxygen species. OM cause deregulation, and injured mitochondrial-mediated ROS generation. OM potently diminished the malondialdehyde level, serum IL-1β and sE-selectin,and caspase-3, and increased levels of glutathione, Bcl-2 by PPAR-γ, NF-κB, and Nrf2/HO-1 Signaling Pathways.