普鲁内拉肉多糖通过阻断TLR介导的NF-κB激活来抑制简单疹病毒感染
Xuanlei Zhong1,2, Yibo Zhang1,2, Man Yuan1,2
1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, No. 1200, Cailun Road, Shanghai, 201203, China.
Chinese medicine
|January 7, 2024
概括
普鲁内拉的多糖 (PVE30) 通过阻断病毒的附着和复制来抑制简单疹病毒 (HSV). 这种强大的抗病毒药物还通过抑制TLR-NF-κB通路抑制炎症和亡.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 自然产品化学 自然产品化学
背景情况:
- 普鲁内拉 (Prunella vulgaris) 聚糖 (PVE30) 对简单疹病毒 (HSV) 具有抗病毒性质.
- 对于PVE30的精确抗HSV机制的理解尚不完全.
研究的目的:
- 阐明PVE30对HSV的抗病毒活性背后的分子机制.
- 研究PVE30对病毒进入,复制和宿主免疫反应的影响.
主要方法:
- 减少斑块的测试确定了抗病毒活性和EC50值.
- 免疫光和肝素珠测定评估了PVE30与病毒葡萄糖蛋白的相互作用.
- 实时PCR,Western blotting和流动细胞计分析了病毒基因和蛋白质表达,TLR-NF-κB通路激活和亡.
主要成果:
- 通过与病毒糖蛋白gB和Cg结合,PVE30竞争性地抑制了HSV的附着,防止了与细胞表面海帕兰硫酸盐的相互作用.
- PVE30降低了早期和晚期病毒基因表达的调节,显著降低了后代病毒产量.
- PVE30抑制了TLR2和TLR3的信号传递,抑制了NF-κB的激活,抑制了促炎性细胞因子 (IL-6,TNF-α) 的产生,并通过MLKL化抑制阻断了HSV-1诱导的亡.
结论:
- 通过抑制病毒的附着和复制,PVE30显示出强大的抗HSV活性.
- PVE30通过阻断TLR介导的NF-κB激活和随后的炎症和亡途径,起到有效的抗病毒作用.
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