基于巨噬细胞焦亡探讨“从脾论治”动脉粥样硬化的科学内涵

Exploring the scientific connotation of ‘treatment from the spleen’ of atherosclerosis based on macrophage pyroptosis

脾属土,居中焦,主运化水谷,若脾失健运,不能正常运化布散水谷精微,多余的脂质沉积于血脉形成痰浊,导致脉道不利,而致动脉粥样硬化(AS)。可见,脾虚生痰是引发AS的关键。巨噬细胞焦亡致AS,其关键为炎症反应。巨噬细胞焦亡释放大量炎症因子,加剧AS进展。中医学将“炎症”归于毒邪范畴,而毒邪可转化为痰浊,并阻滞血脉,导致脉道不利,形成AS。这与炎症反应所致AS的过程基本一致,可见脾虚生痰和巨噬细胞焦亡对于AS均具有重要意义。应用健脾祛痰中药干预,以巨噬细胞焦亡为切入点,以microRNA-221/NLRP3/Caspase-1信号通路为关键环节入手,探究脂质水平、炎症因子、血管内皮结构改变、microRNA-221/NLRP3/Caspase-1信号通路的调控等改变,阐明健脾祛痰中药影响巨噬细胞焦亡抗AS的分子机制,为中医临床“从脾论治”AS性疾病提供实验依据。

The spleen belongs to soil, which is in the middle of the coke. If the spleen fails to function properly, it cannot transport and disperse the water grains. The excess lipid will deposit in the blood vessels to form turbid phlegm, which will lead to the adverse pulse channels and lead to atherosclerosis(AS). It can be seen that spleen deficiency and phlegm production is the key to cause as. Inflammation is the key to AS caused by macrophage scorch. Macrophage pyrosis releases a large number of inflammatory factors, which aggravates the progress of AS. Traditional Chinese medicine puts ‘inflammation’ in the category of toxin, which can transform into turbid phlegm and block blood vessels, resulting in adverse pulse channels and forming AS. This is basically consistent with the process of AS caused by inflammatory reaction. It can be seen that spleen deficiency producing phlegm and macrophage pyroptosis are of great significance to AS. In order to explore the lipid level, inflammatory factors,vascular endothelial structure changes, and microRNA-221/NLRP3/Caspase-1 signaling pathway, we used Jianpi Qutan traditional Chinese medicine intervention, with macrophage death as the breakthrough point, and microRNA-221/NLRP3/Caspase-1 signaling pathway as the key link. The regulation of Caspase-1 signaling pathway and other changes will clarify the molecular mechanism of spleen invigorating and expectorant Chinese medicine affecting macrophage pyroptosis and anti-AS, and provide experimental basis for clinical treatment of AS disease from spleen.