Pharmacological intervention of curcumin via the NLRP3 inflammasome in ischemic stroke

Abstract

Ischemic-induced neuronal injury arises due to low oxygen/nutrient levels and an inflammatory response that exacerbates neuronal loss. NOD-like receptor family pyrin domain-containing 3 (NLRP3) is an important regulator of inflammation after ischemic stroke, with its inhibition being involved in nerve regeneration. Curcumin, a main active ingredient in Chinese herbs, plays a positive role in neuronal repair and neuroprotection by regulating the NLRP3 signaling pathway. Nevertheless, the signaling mechanisms relating to how curcumin regulates NLRP3 inflammasome in inflammation and neural restoration following ischemic stroke are unknown. In this report, we summarize the main biological functions of the NLRP3 inflammasome along with the neuroprotective effects and underlying mechanisms of curcumin via impairment of the NLRP3 pathway in ischemic brain injury. We also discuss the role of medicinal interventions that target the NLRP3 and potential pathways, as well as possible directions for curcumin therapy to penetrate the blood–brain barrier (BBB) and hinder inflammation in ischemic stroke. This report conclusively demonstrates that curcumin has neuroprotective properties that inhibit inflammation and prevent nerve cell loss, thereby delaying the progression of ischemic brain damage.

Integrating hydrogels manipulate ECM deposition after spinal cord injury for specific neural reconnections via neuronal relays

“…Prolonged release of NT3 from HADA/HRR-based hydrogels improved the adjacent microenvironment, promoting the survival of resident neurons. In addition to immunoregulation effects, Cur has been recently demonstrated to play a positive role in neuronal repair and neuroprotection ( 43 ). Therefore, Cur also contributed to the enhancement of neuronal survival.…”

Novel Multi-Antioxidant Approach for Ischemic Stroke Therapy Targeting the Role of Oxidative Stress

“…The NLRP3 inflammasome, extensively studied in stroke models, responds to danger signals such as ROS generated during ischemia-reperfusion. Activation of NLRP3 leads to increased production of proinflammatory cytokines such as IL-18 or IL-1β [ 31 ]. Similarly, NLRP1, another member of the NLR family, contributes to neuroinflammation by forming its inflammasome complex.…”