Resveratrol acts through the NF-κB/STAT3 signaling pathway to alleviate lead-induced neuroinflammatory pathology in mice Reference Data
Description
Resveratrol, a natural polyphenol, has garnered significant attention due to its potential neuroprotective properties in various models of neurodegenerative diseases. This study investigated the neuroprotective effects of resveratrol (RES) against lead-induced neuroinflammatory injury in a mouse model, focusing on its role in regulating amyloid-beta (Aβ) aggregation, glial cell activation, and neuroinflammatory pathways. Lead exposure significantly increased Aβ expression in hippocampal subregions CA1, CA3, and DG by 87.6-fold, 39.8-fold, and 19.9-fold, respectively P < 0.05), and by 36.8-fold in the cerebral cortex. RES treatment considerably lowered Aβ levels by up to 73.6%, 68.4%, and 61.3% in these hippocampal areas and by 74.8% in the cortex (P < 0.05). Likewise, markers of microglial activation (Iba1) and astrocyte activation (GFAP) showed significant increases after lead exposure, and RES reduced these markers by over 60% in most brain regions (P < 0.05), indicating suppression of glial overactivation. RES also inhibited key pro-inflammatory pathways: NF-κB expression increased by 64.8% in lead-treated mice but was decreased by 16-23% following RES administration (p < 0.05). Phosphorylated STAT3 signaling, which rose by 73.6% due to lead exposure, was decreased by up to 40.7% with RES intervention (p < 0.05). Western blot, immunofluorescence staining, H&E staining, and Nissl staining results were performed using ImageJ software. All experimental data were analyzed by one-way ANOVA and plotted using GraphPad Prism v.10, and are presented as mean ± SEM. A value of *P < 0.05 was considered statistically significant.