Proanthocyanidins alleviate Henoch‐Schönlein purpura by mitigating inflammation and oxidative stress through regulation of the TLR4/MyD88/NF‐κB pathway

Abstract

AbstractObjectiveInvestigate Proanthocyanidins (PCs) efficacy and mechanisms in treating Henoch‐Schönlein purpura (HSP)‐like rat models, focusing on inflammatory and oxidative stress (OS) responses.MethodsAn HSP‐like rat model was established using ovalbumin (OVA) injection, leading to symptoms mimicking HSP. The study measured inflammatory markers (IL‐4, IL‐17, TNF‐α), OS markers (MDA, SOD, CAT), and assessed the TLR4/MyD88/NF‐κB signaling pathway's involvement via histopathological and immunofluorescence analyses.ResultsPCs treatment significantly improved HSP‐like symptoms, reduced inflammatory cell infiltration, and decreased IgA deposition in renal mesangial areas. Serum analyses revealed that PCs effectively lowered IL‐4, IL‐17, TNF‐α, and MDA levels while increasing SOD and CAT levels (p < 0.05). Crucially, PCs also downregulated TLR4, MyD88, and NF‐κB expressions, highlighting the blockage of the TLR4‐mediated signaling pathway as a key mechanism.ConclusionPCs show promising therapeutic effects in HSP‐like rats by mitigating inflammatory responses and oxidative damage, primarily through inhibiting the TLR4/MyD88/NF‐κB pathway. These findings suggest PCs as a potential treatment avenue for HSP, warranting further investigation.