Benidipine Hydrochloride Inhibits NLRP3 Inflammasome Activation by Inhibiting LPS-Induced NF-κB Signaling in THP-1 Macrophages

NLRP3, ASC, and procaspase-1 form the multiprotein complex known as the NLRP3 inflammasome. Following the priming of NLRP3 by TLR4 ligand, the activation of the NLRP3 inflammasome causes caspase-1 maturation, which results in the release of IL-1β. Calcium channel antagonists are commonly employed as antihypertensive medications and have anti-inflammatory properties through the inhibition of cytokine release, specifically IL-1β. The impact of calcium channel antagonists on NLRP3 inflammasomes, however, has not been well studied. This study aimed to investigate the effect of the calcium channel blocker benidipine hydrochloride on LPS-induced NLRP3 inflammasome activation in THP-1 macrophages and its possible mechanism.