竹节参总皂苷改善高脂高糖饮食小鼠的神经炎症及可能的机制

Improvement of Neuroinflammation in Mice Induced By High-Fat-High-Fructose Diet by Saponins of Panax Japonicus and the Possible Underlying Mechanism

摘要:

探索了竹节参总皂苷(saponins of Panax Japonicus，SPJ)对高脂高糖饮食诱导小鼠脑组织炎症反应的改善效果。Balb/c小鼠随机分为四组：正常对照组、模型对照组、SPJ低剂量组（16.7 mg/kg），SPJ高剂量组（50 mg/kg），分别给予普通饲料、高脂高糖饲料及添加不同剂量SPJ的高脂高糖饲料，喂养4个月。与正常对照组比较，模型对照组的皮层形态结构异常，细胞凋亡增多，小胶质细胞激活增加，炎症相关因子表达升高。给予竹节参总皂苷干预，可明显改善脑组织形态结构，减少细胞凋亡和小胶质细胞活化，减轻炎症相关因子iNOS、COX-2和IL-1β的蛋白表达，并抑制NLRP3炎症小体包括NLRP3、ASC、Caspase-1的表达。可见，竹节参总皂苷可具有改善高脂高糖饮食小鼠的脑组织炎症反应的效果，其机制可能与抑制NLRP3炎症小体的激活从而减少炎症因子表达有关。

Abstract:

The effects of saponins of Panax japonicus (SPJ) on the inflammatory response in the brain tissue of mice induced by high-fat-high-fructose diet (HFFD) were investigated. Balb/c mice were randomly divided into following groups: normal control group, model control group, SPJ-treated groups. Normal control mice were fed with standard diet, while model control group were fed with HFFD, and SPJ-treated groups were fed with HFFD combined with low-dose SPJ (16.7 mg/kg) and high dose SPJ (50 mg/kg) for 4 months. Compared with the normal control group, model control group exhibited increased cell apoptosis and microglia activation. Meanwhile, protein expression levels of inflammatory-related factors were significantly increased. Treatment mice with SPJ significantly improved the morphology and structure of brain tissue, inhibited neuronal cell apoptosis and microglia activation. In addition, SPJ significantly decreased the protein levels of inflammatory related factors such as iNOS, COX-2 and IL-1β, and inhibited the activation of NLRP3 inflammasome including NLRP3, ASC and Caspase-1. Thus, SPJ could improve the inflammatory response of brain tissue induced by HFFD, and its underlying mechanism might related to inhibition of the activation of NLRP3 inflammasome, leading to reduced expression levels of inflammatory factors.