Baicalin alleviates lead-induced cognitive dysfunction by modulating apoptosis and autophagy in mice

作者：Yu Jia, Dahai Yu, Yong Pang, Weiyun Zhang, Shuang Liu, Xuexun Fang, Jie Zhang · 发表于：Ecotoxicology and Environmental Safety · 年份：2025 · DOI：10.1016/j.ecoenv.2025.119549 · 被引用次数：1 · 研究领域：Flavonoids in Medical Research、Autophagy in Disease and Therapy、Saffron Plant Research Studies

Lead exposure is a well-documented environmental neurotoxin that poses a persistent threat to brain development. Excessive lead accumulation in this region impairs cognitive function and induces neuronal damage, yet effective therapeutic interventions remain limited. Baicalin, a flavonoid compound derived from Scutellaria baicalensis, exhibits antioxidant and neuroprotective activity, but its efficacy against lead-induced neural injury has not been fully elucidated. Here, we established a subchronic lead exposure model in mice and administered baicalin orally following lead treatment. Cognitive function was assessed through spatial, recognition, and avoidance learning paradigms. Lead concentrations in blood and hippocampus, as well as hippocampal structural integrity, oxidative stress markers, apoptosis signals, and neuronal autophagy, were quantitatively analyzed. In vitro studies using HT22 cells further investigated the effects of baicalin on oxidative stress, mitochondrial function, and autophagy-related signaling pathways. Baicalin treatment significantly improved cognitive performance, reduced blood and hippocampal lead concentrations, preserved hippocampal morphology, and reestablished redox homeostasis. Baicalin reduced lipid peroxidation, suppressed neuronal apoptosis, and restored autophagic flux. Mechanistically, baicalin activated AMPK, inhibited mTOR phosphorylation, and promoted ULK1-mediated autophagy. These effects were abolished by pharmacological inhibition ...