Naringenin Produces Neuroprotection Against LPS-Induced Dopamine Neurotoxicity via the Inhibition of Microglial NLRP3 Inflammasome Activation

Conclusions: This study demonstrated that NAR targeted microglial NLRP3 inflammasome to protect DA neurons against LPS-induced neurotoxicity. These findings suggest NAR might hold a promising therapeutic potential for PD. Background Parkinson's disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. It is characterized by slow and progressive loss of dopamine (DA) neurons in the midbrain substantia nigra (SN) with the accumulation of α-synuclein in Lewy bodies and neuritis (1). Although the etiology of PD remains unclear, amounts of studies have suggested that neuroinflammation is recognized as the major central event in the process of DA neuronal cell death in PD (2). The hallmark of neuroinflammation is glial activation, especially microglia activation. Microglia are the chief innate immune cells within the CNS. Upon the introduction of stimuli, such as brain injury, inflammation and pathogens, microglia became activated and released a large number of neurotoxic factors, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-18, and then these factors would work in concert to trigger neurodegeneration (3). Among these inflammatory factors, IL-1β was considered to be indispensable for the initiation and progress of DA neurodegeneration (4). Postmortem studies demonstrated that enhanced IL-1β expression was discerned in the microglia surrounding Lewy b...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research