葛根素抗内毒素血症小鼠血管内皮损伤的作用及其机制

Effect and mechanism of puerarin on vascular endothelial injury in mice with endotoxemia

目的探讨葛根素抗内毒素血症小鼠血管内皮损伤的作用及其机制。方法将18只BALB/C小鼠随机分为正常对照组,LPS组,葛根素组。ELISA法检测血清中肿瘤坏死因子-α(TNF-α),白细胞介素-1β(IL-1β),白细胞介素-6(IL-6),细胞间黏附分子-1(ICAM-1),血管细胞间黏附分子-1(VCAM-1)和E-选择素(E-selectin)的含量;左肺组织行HE染色进行病理学观察,右肺组织测湿干重比。结果与正常对照组比,LPS组小鼠血清中炎症因子TNF-α和IL-1β以及黏附分子ICAM-1,VCAM-1和E-selectin水平明显升高,IL-6变化不明显,肺湿干重比增加,肺组织间隔增宽,炎症细胞浸润。与LPS组相比,葛根素组小鼠血清中炎症因子TNF-α和IL-1β以及黏附分子ICAM-1,VCAM-1和E-selectin水平明显降低,IL-6变化不明显,肺湿干重比下降,肺组织间隔增宽程度降低,炎症细胞浸润减少。结论葛根素预处理可明显减轻LPS所致内毒素血症小鼠血管内皮损伤,其机制可能与降低炎症因子和黏附分子水平有关。

Objective To investigate the effect of puerarin on vascular endothelial injury in mice with endotoxemia. Methods Eighteen BALB/C mice were randomly divided into normal control group, endotoxemia group (LPS group) and puerarin group.The contents of tumor necrosis factor-α(TNF-α), interleukin-1 β(IL-1β), interleukin-6(IL-6), intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1) and E-selectin (E-selectin) were detected by ELISA;the left lung tissue was determined by HE staining for pathological observation, the right lung tissue was measured the ratio of wet to dry weight. Results Compared with the normal control group, the levels of inflammatory factors TNF-αand IL-1 β as well as adhesion molecules ICAM-1, VCAM-1 and E-selectin in the serum of LPS group were significantly increased, but IL-6 was not.The ratio of wet to dry weight was increased.The lung tissue interval was widened and inflammatory cells infiltrated in LPS group.Compared with the LPS group, the levels of inflammatory factors TNF-α and IL-1 β as well as adhesion molecules ICAM-1, VCAM-1 and E-selectin in the serum of puerarin group were significantly decreased, while IL-6 was not.The ratio of wet to dry weight was decreased.The lung tissue interval was narrowed and the inflammatory cell filtration was reduced. Conclusions Pretreatment with puerarin can significantly reduce vascular endothelial injury in mice with endotoxemia, thereby protecting the lung.