木犀草素
神经炎症
神经保护
药理学
芹菜素
小胶质细胞
黄芩素
AKT1型
医学
细胞凋亡
蛋白激酶B
类黄酮
化学
炎症
免疫学
生物化学
抗氧化剂
作者
Min-Rui Ding,Chenbo Xia,Yan-Jie Qu,Li-Min Zhang,Mengxue Zhang,Rong-Rong Zhen,Tong Zhang,Jin-Fang Chen,Bing Hu,Hongmei An
标识
DOI:10.1142/s0192415x25500806
摘要
Alzheimer’s disease (AD) currently lacks effective therapeutics, but blood–brain-barrier-penetrating flavonoids show promising therapeutic potential. To address this critical need, we employed a novel network medicine framework to systematically identify flavonoid compounds for AD therapy by quantifying their network proximity to AD targets. Our systematic screening identified 48 potential anti-AD flavonoids, of which luteolin, quercetin, apigenin (API), and baicalein demonstrated significant neuroprotective effects in A[Formula: see text]25–35-induced rat pheochromocytoma (PC12) cell models. Of these, API emerged as the most promising candidate. A network pharmacological analysis revealed that API likely exerts its anti-AD effects through modulating apoptosis and inflammatory response, and AKT1 and NFKBIA were identified as key therapeutic targets. Experimental validation demonstrated that API treatment impeded the H 2 O 2 -induced decline in the mitochondrial membrane potential of PC12 cells, suppressed apoptosis, and mitigated neuronal damage. Furthermore, API downregulated the AKT/NF-[Formula: see text]B signal pathway, promoted microglial M2 polarization, and attenuated LPS-induced neuroinflammation in BV2 cells. API also alleviated the toxic effects of M1 microglia on neurons. This network-based screening strategy provides an innovative approach for developing new AD therapeutics.
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