Regulatory Mechanism of Vitexin on Cell Pyroptosis Mediated by AMPK/NLRP3 Pathway in Acute Pharyngitis Rats
Objective:This study aimed to investigate the effects of vitexin on acute pharyngitis in rats and its regulatory mechanism through the AMPK/NLRP3 signaling pathway.Methods:Sixty SD rats were randomly divided into control,model,amoxicillin groups,and low,medium,and high dose vitexin groups,with 10 rats per group.Except for the control group,acute pharyngitis models were established in the remaining groups by targeted spraying of 25%ammonia water into the throat.Rats in vitexin groups received intraperitoneal injections of 3,6,or 12 mg/kg vitexin,while those in the amoxicillin group were administered 0.36 g/kg orally.The remaining rats received an equivalent volume of 0.9%saline intraperitoneally.After 7 days of intervention,behavioral scoring,pathological staining of throat tissues,and serum inflammatory factors IL-6,IL-1β,TNF-α,and PGE2 were measured to determine the optimal dose of vitexin.Protein expression related to cell pyroptosis and AMPK/NLRP3 in throat tissues was also evaluated.Subsequently,40 SD rats were randomly divided into control,model,vitexin(intraperitoneal injection of 12 mg/kg vitexin),and vitexin+CC(AMPK inhibitor)groups,with 10 rats per group.Acute pharyngitis models were induced in all groups except the control,followed by drug interventions(once daily for 7 days).Throat tissue pathology was observed using Hematoxylin-Eosin(HE)staining,serum levels of IL-6,IL-1β,TNF-α,and PGE2 were measured using enzyme-linked immunosorbent assay(ELISA),and AMPK/NLRP3 pathway-related protein and cell pyroptosis-related protein expression were detected using Western blot.Results:Compared with the model group,behavioral scores of rats in vitexin groups significantly decreased(P<0.05),serum IL-6,IL-1β,TNF-α,and PGE2 levels were reduced(P<0.05),and pathological damage in throat tissues was significantly alleviated in a dose-dependent manner.The optimal dose of vitexin was determined to be 12 mg/kg.Compared with the model group,rats in the vitexin group showed significantly increased p-AMPK protein positivity,decreased NLRP3 protein positivity,and reduced expression of cell pyroptosis-related proteins(P<0.05).Compared with the vitexin group,rats in the vitexin+CC group exhibited exacerbated throat tissue damage,increased serum IL-6,IL-1β,TNF-α,and PGE2 levels,elevated cell pyroptosis-related protein and NLRP3 protein expression,and decreased p-AMPK/AMPK ratio(P<0.05).Conclusion:Vitexin can improve acute pharyngitis in rats by inhibiting cell pyroptosis through the regulation of the AMPK/NLRP3 signaling pathway.
Acute pharyngitisVitexinAdenosine monophosphate-activated protein kinase/nucleotide-binding oligomerization domain-like receptor protein 3 pathwayCell pyroptosis
万方数据
维普
