Inhibition o. The TLR/NF- κ B Signaling Pathway and Improvement of Autophagy Mediates Neuroprotective Effects of Plumbagin in Parkinson's Disease

Abstract

A naphthoquinone molecule known as plumbagin (PL), which has a wide range of pharmacological properties including antitumor, antioxidation, anti-inflammation, and neuroprotective effects, is extracted fro. The roots o. The medicinal herb Plumbago zeylanica L. Plumbagin has been studied for its potential to treat Parkinson's disease (PD). However, its effectiveness and mechanism are still unknown. This study intends to evaluate plumbagin's effectiveness against PD in vitro and in vivo. Plumbagin partially repaire. The loss of dopaminergic neurons i. The nigral substantia nigra an. The resulting behavioural impairment caused by MPTP or MPTP/probenecid in mice. Furthermore, plumbagin treatment significantly inhibite. The TLR/NF-κB pathways. It reduce. The TNF-α, IL-6, and IL-1β mRNA expression in PD mice induced by MPTP or MPTP/probenecid, which was consistent wit. The findings i. The inflammatory model of BV2 cells induced by MPP+ or LPS. In addition, plumbagin treatment enhance. The microtubule-associated protein 1 light chain 3 beta (LC3) LC3-II/LC3-I levels while decreasin. The p-mTOR and p62 protein accumulation in PD mice induced by MPTP or MPTP/probenecid, which was similar t. The results obtained fro. The experiments in SH-SY5Y and PC12 cells induced by MPP+. Consequently, our results suppor. The hypothesis that plumbagin, by promoting autophagy and inhibitin. The activation o. The TLR/NF-κB signaling pathway, is a promising treatment agent for treating Parkinson's disease (PD). However, to confirm plumbagin's anti-PD action more thoroughly, other animal and cell PD models must be used in future studies.