Abstract
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common neurodegenerative diseases. Many studies have demonstrated that the release of NLRP3 inflammasome-mediated proinflammatory cytokines by the excessive activation of microglia is associated with the pathogenesis of AD and PD and suggested that the NLRP3 inflammasome plays an important role in AD and PD development. In both diseases, various stimuli, such as Aβ and α-synuclein, accelerate the formation of the NLRP3 inflammasome in microglia and induce pyroptosis through the expression of interleukin (IL)-1β, caspase-1, etc., where neuroinflammation contributes to gradual progression and deterioration. However, despite intensive research, the exact function and regulation of the NLRP3 inflammasome has not yet been clearly identified. Moreover, there have not yet been any experiments of clinical use, although many studies have recently been conducted to improve treatment of inflammatory diseases using various inhibitors for NLRP3 inflammasome pathways. However, recent studies have reported that various natural products show improvement effects in the in vivo models of AD and PD through the regulation of NLRP3 inflammasome assembly. Therefore, the present review provides an overview of natural extraction studies aimed at the prevention or treatment of NLRP3 inflammasome-mediated neurological disorders. It is suggested that the discovery and development of these various natural products could be a potential strategy for NLRP3 inflammasome-mediated AD and PD treatment.
Highlights
Neuroinflammation, an inflammatory response that occurs in the damaged central nervous system, is an important factor in neurodegeneration
Persistent inflammation that occurs during the pathogenesis of various neurological disorders in the central nervous system is mediated by activation of the NLRP3 inflammasome, a key innate immune sensor that is associated with the progression of several neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), traumatic brain injury, stroke, depression, and multiple sclerosis [3,4]
The reduction in Aβ deposition was not significant, baicalin reduced microglia activation, IL-18, IL-1β, and iNOS expression in APP/PS1 mice and LPS/Aβ-stimulated BV2 cells. These results indicated the protective effects of baicalin in AD progression were related to the inhibition of microgliainduced neuroinflammation by suppressing the activation of NLRP3 inflammasomes and the toll-like receptor 4 (TLR4)/NF-κB signaling pathway [51]
Summary
Jun Ho Lee 1 , Hong Jun Kim 1 , Jong Uk Kim 1 , Tae Han Yook 1 , Kyeong Han Kim 1 , Joo Young Lee 2 and Gabsik Yang 1, *.
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