摘要
目的:观察黄芪多糖(APS)对脓毒症大鼠肺血管内皮细胞的保护作用,并探讨可能机制。方法:采用盲肠结扎穿孔法建立脓毒症大鼠模型,将建模成功的36只大鼠随机分为脓毒症组、APS组、APS+脂多糖(LPS)组,每组各12只。另外12只大鼠设为对照组。术后6、12、18h APS组灌胃APS(100mg/kg),APS+LPS组灌胃APS(100mg/kg)+腹腔注射LPS(3mg/kg),对照组、脓毒症组分别灌胃、腹腔注射等量生理盐水。检测血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平;检测肺组织含水量、Western Blotting法检测肺组织中热休克蛋白70(HSP70)、内皮细胞特异性分子-1(ESM-1)蛋白,Toll样受体4(TLR4)、髓样细胞分化因子88(MyD88)、核转录因子-κB p65(NF-κB p65)、p-NF-κB p65蛋白表达量。结果:与脓毒症组比较,APS组血清IL-6、TNF-α水平,肺组织含水量,ESM-1蛋白表达量,肺组织TLR4、MyD88蛋白表达量,p-NF-κB p65/NF-κB p65均降低(P<0.05),HSP70蛋白表达量升高(P<0.05);与APS组比较,APS+LPS组血清IL-6、TNF-α水平,肺组织含水量,ESM-1蛋白表达量,肺组织TLR4、MyD88蛋白表达量,p-NF-κB p65/NF-κB p65均升高(P<0.05),HSP70蛋白表达量降低(P<0.05)。结论:APS可能通过抑制TLR4/NF-κB通路减轻脓毒症大鼠炎症反应及肺损伤,保护肺血管内皮细胞。
Objective:To observe the protective effect of astragalus polysaccharide(APS)on pulmonary vascular endothelial cells in sepsis rats,and to explore the possible mechanism.Method:Sepsis rat model was established by cecal ligation and perforation.36 rats were randomly divided into sepsis group,APS group and APS+lipopolysaccharide(LPS)group,12 rats in each group.The other 12 rats were served as the control group.At 6,12 and 18h after operation,APS group was intragastric administration of APS(100mg/kg),APS+LPS group was intragastric administration of APS(100mg/kg)+intraperitoneal injection of LPS(3mg/kg),control group and sepsis group were intragastric administration and intraperitoneal injection of equal amount of normal saline solution,respectively.Serum levels of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were detected.The water content of lung tissue was detected,and the expression of heat shock protein 70(HSP70),endothelial cell specific molecular-1(ESM-1)protein,Toll-like receptor 4(TLR4),myeloid cell differentiation factor 88(MyD88),nuclear transcription factor-κB p65(NF-κB p65)and p-NF-κB p65 protein in the tissue were detected by Western blot.Results:Compared with sepsis group,serum IL-6 and TNF-αlevels,lung tissue water content,ESM-1 protein expression,lung TLR4,MyD88 protein expression,p-NF-κB p65/NF-κB p65 protein expression were decreased in APS group(P<0.05),and HSP70 protein expression was increased(P<0.05).Compared with APS group,serum IL-6 and TNF-αlevels,lung tissue water content,ESM-1 protein expression,lung TLR4,MyD88 protein expression,P-NF-κB p65/NF-κB p65 were increased in APS+LPS group(P<0.05).The expression of HSP70 protein was decreased(P<0.05).Conclusion:APS alleviates inflammation and lung injury in sepsis rats and protects pulmonary vascular endothelial cells,possibly by inhibiting TLR4/NF-κB pathway.
作者
徐曼
沈月
米妍妍
王春双
周海岩
XU Man;SHEN Yue;MI Yan-yan;WANG Chun-shuang;ZHOU Hai-yan(The Third Department of Critical Medicine,Baoding First Central Hospital,Baoding 071000,China)
出处
《微循环学杂志》
2023年第3期6-11,共6页
Chinese Journal of Microcirculation
基金
保定市科技计划项目(2141ZF070)。
关键词
黄芪多糖
脓毒症
肺血管内皮细胞
肺损伤
Astragalus polysaccharide
Sepsis
Pulmonary vascular endothelial cells
Lung injury
