Mechanism of total Ginkgo biloba flavone mediating the inflammation and autophagy in lipopolysaccharide-induced human coronary artery endothelial cells through TLR4/PI3K signaling pathway

作者：Yudan Wen, Wenwen Lin, Weiwei Wang · 发表于：Journal of Radiation Research and Applied Sciences · 年份：2025 · DOI：10.1016/j.jrras.2025.101712 · 被引用次数：3 · 研究领域：Ginkgo biloba and Cashew Applications、Neurological Disease Mechanisms and Treatments、Nuclear Receptors and Signaling

Objective The mechanism of total Ginkgo biloba flavonoids (GBF) on lipopolysaccharide (LPS)-induced inflammation damage and excessive autophagy in human coronary artery endothelial cells (HCAECs) was investigated. Methods Total GBF was extracted, and its scavenging abilities for DPPH·, ABTS+, and ·OH free radicals were assessed. LPS-stimulated HCAECs served as the atherosclerotic inflammatory model (control). Treatment groups received total GBF extracts at 1 (LD-GBF), 10 (MD-GBF), or 100 μg/mL (HD-GBF). Cell proliferation and apoptosis rates were measured. Interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF-α) levels and immunofluorescence staining was implemented for examining the light chain 3 beta (LC3B) level in HCAECs. Protein imprinting examined the expressions of LC3B, Beclin1, Toll-like receptor 4 (TLR4), and phosphatidylinositol 3-kinase (PI3K). Results Total GBF scavenged the DPPH·, ABTS+, and ·OH free radicals, with half-inhibitory concentrations of 0.65, 0.12, and 0.38 mg/mL, respectively. LPS group exhibited reduced cell proliferation vitality, increased cell apoptosis rate, elevated IL-6, IL-8, and TNF-α, and downregulated LC3B II/I, Beclin1 versus control group ( P < 0.05). LPS upregulates TLR4 and PI3K, while GBF dose dependently reduced their expression. LD-GBF, MD-GBF, and HD-GBF groups demonstrated increased cell proliferation vitality, decreased cell apoptosis rate, lowered IL-6, IL-8, and TNF-α, and reduced downregulated LC3B II/I, Beclin1, TLR4, a...