In acquired and neurodegenerative brain diseases, inflammation-mediated neuronal death contributes to the deterioration of neurological deficits in patients. In the innate immune system, the NLRP3 inflammasome is a cytosolic complex that regulates the release of pro-inflammatory cytokines IL-1β and IL-18, thereby amplifying the inflammatory response and neuronal damage. Consequently, inhibition of NLRP3 inflammasome represents a promising pharmacological strategy to limit inflammation across multiple pathologies. Oxidative stress is a common hallmark of these pathological conditions, that contribute to neuronal death and influencing NLRP3 activation. Despite the implications of these events, the molecular mechanisms underlying this activation remain poorly understood. In this review, we describe the key features of the NLRP3 inflammasome and explore the role of oxidative stress in its activation. Additionally, we discuss the evidence supporting the regulation of inflammasome activity by antioxidant molecules. Understanding the role of oxidative stress in NLRP3-mediated inflammation offers promising advantages for therapeutic strategies to reduce neuronal death.
Ramirez-Celis et al. (Sat,) studied this question.