姬松茸多糖对LPS诱导人脐静脉血管内皮细胞损伤的保护机制

目的：探讨姬松茸多糖（ABP）对脂多糖（LPS）诱导的人脐静脉血管内皮细胞（HUVECs）损伤的保护作用及其可能的机制。方法：HUVECs分为Control组、LPS组（终浓度为1 μg/mL LPS构建细胞损伤模型）、LPS+ABP组（LPS基础上分别用10、20、50 μg/mL ABP进行干预），CCK-8法检测ABP对HUVECs的细胞毒性作用，ELISA法、Western blot及RT-PCR检测各组炎症因子及细胞黏附分子的表达，Western blot和免疫荧光法检测各组NF-κB信号通路相关蛋白表达及核转位。结果：LPS组TNF-α、IL-6、COX-2、iNOS、ICAM-1、VCAM-1蛋白及p-p65/p65、p-IκB/IκB蛋白相对表达量较Control组显著升高（P ＜0.01）；LPS+ABP组随药物浓度升高，TNF-α、IL-6、COX-2、iNOS、ICAM-1、VCAM-1蛋白及p-p65/p65、p-IκB/IκB蛋白表达较LPS组逐渐降低（P ＜0.05）。LPS组TNF-α、IL-6、COX-2、iNOS、ICAM-1、VCAM-1 mRNA较Control组显著升高（P ＜0.01）；LPS+ABP组随药物浓度升高，TNF-α、IL-6、COX-2、iNOS、ICAM-1、VCAM-1 mRNA表达较LPS组逐渐降低（P ＜0.05）。结论：ABP可以通过抑制LPS诱导的炎症因子和细胞黏附分子的表达来减轻HUVECs的损伤，其机制可能与抑制细胞中NF-κB信号通路的激活有关。

Protective effect of agaricus blazei polysaccharide on LPS-induced injury of human umbilical vein endothelial cells and its mechanism

Objective: To investigate the protective effect of Agaricus blazei Murrill polysaccharide (ABP) on the injury of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS) and its possible mechanism. Methods: The cell damage model was constructed with LPS at a final concentration of 1 μg/mL and divided into control group, LPS group, and ABP intervention group (10, 20, 50 μg/mL). CCK-8 method was used to detect the effects of ABP on HUVECs. Cytotoxicity, ELISA, Western blot and RT-PCR were used to detect the expression of inflammatory factors and cell adhesion molecules in each group. Western blot and immunofluorescence were used to detect the expression of proteins related to the NF-κB signaling pathway and nuclear translocation in each group. Results: The relative expressions of TNF-α, IL-6, COX-2, iNOS, ICAM-1, VCAM-1, p-p65/p65, p-IκB/IκB protein in LPS group were significantly higher than those in control group (P<0.01). With the increase of drug concentration, the expression of above proteins in ABP group were significantly lower than that in LPS group (P<0.05). RT-PCR detection showed that TNF-α, IL-6, COX-2, iNOS, ICAM-1 and VCAM-1 mRNA expressions in LPS group were significantly higher than those in control group (P<0.01). With the increase of drug concentration, the expression of above-mentioned mRNA expressions in ABP group were significantly lower than that in LPS group (P<0.05). Conclusion: ABP can inhibit the expression of inflammatory factors and cell adhesion molecules induced by LPS to reduce the damage of HUVECs. The mechanism may be related to the inhibition of the activation of NF-κB signaling pathway in cells.