Curcumin Ameliorates Microplastic-Induced Testicular Inflammatory Damage by Suppressing NLRP3 and WNT/β-Catenin Signaling Pathway Activation

Background.While the reproductive toxicity of microplastics (MPs) and associated mechanisms have been extensively documented, the specific signaling pathways underlying MPs-induced testicular injury remain incompletely elucidated.Current studies focus on identifying molecular mechanisms by which MPs disrupt testicular homeostasis through inflammatory and developmental signaling cascades.Methods.This study investigated the molecular mechanisms of MPs-induced testicular injury using a rodent model exposed to environmentally relevant concentrations of MPs.The synergistic roles of the NLRP3 inflammasome and WNT/-catenin signaling pathways in mediating inflammatory damage were analyzed through biochemical assays, cytokine profiling, and histopathological evaluation.The therapeutic potential of curcumin was assessed by measuring its effects on NLRP3 inflammasome activation, WNT pathway hyperactivation, and functional recovery of Sertoli cells.Results.MPs exposure triggered NLRP3 inflammasome assembly and IL-6 release, initiating a localized inflammatory cascade.Concurrently, MPs activated the WNT/-catenin pathway, disrupting spermatogenic microenvironment homeostasis and exacerbating testicular tissue injury.Curcumin treatment suppressed NLRP3 inflammasome activation, blocked inflammatory cytokine release, and downregulated key WNT pathway effectors.These interventions restored Sertoli cell physiological function and mitigated MPsinduced structural damage.Conclusion.This study reveals a novel mechanism by which MPs induce testicular injury through synergistic activation of NLRP3 and WNT/-catenin pathways, and demonstrates curcumin's efficacy as a multi-target therapeutic agent.The findings provide critical insights into environmental pollutant-induced reproductive toxicity and highlight the potential of natural compounds in clinical intervention.Future research should explore crosstalk between these pathways and validate translational strategies for human applications.