穿心莲内酯减轻血栓闭塞性脉管炎大鼠血管内皮炎症OA
Andrographolide attenuates vascular endothelial inflammation in rats with thromboangiitis obliterans
目的:探讨穿心莲内酯(AP)对血栓闭塞性脉管炎(TAO)大鼠血管内皮炎症及高迁移率族蛋白1(HMGB1)/晚期糖基化终末产物受体(RAGE)信号通路的影响.方法:构建TAO大鼠模型,将造模成功大鼠随机分为模型组(TAO组),AP低、高剂量组(AP-L、AP-H组)、AP高剂量+通路激活剂组(AP-H+rHMGB1组),每组12只,另取12只正常大鼠作为对照组;对各组大鼠TAO病变进行分级评分;血液黏度仪测定全血黏度和血浆黏度;ELISA检测血栓形成因子水平;H-E染色观察股动脉病理形态;免疫印迹检测血管内皮炎症因子及HMGB1/RAGE信号通路相关蛋白表达.结果:TAO组较对照组股动脉血管内皮细胞脱落严重,有大量血栓形成,全血黏度、血浆黏度、血栓烷B2(TXB2)水平及白细胞介素-6(IL-6)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、HMGB1、RAGE、p-NF-κB p65/NF-κB p65表达升高,6-酮-前列腺素F1α(6-Keto-PGF1α)水平降低;AP-L、AP-H组较TAO组股动脉血管内皮细胞脱落减轻,少量血栓形成,全血黏度、血浆黏度、TXB2水平及IL-6、ICAM-1、VCAM-1、HMGB1、RAGE、p-NF-κB p65/NF-κB p65表 达 降 低,6-Keto-PGF1α水平升高;AP-H+rHMGB1组较AP-H组股动脉血管内皮细胞脱落加重,血栓形成增多,全血黏度、血浆黏度、TXB2水平及IL-6、ICAM-1、VCAM-1、HMGB1、RAGE、p-NF-κB p65/NF-κB p65表 达 升 高,6-Keto-PGF1α水平降低.结论:AP可减轻TAO大鼠血管内皮炎症,其作用机制与抑制HMGB1/RAGE信号通路相关.
Objective:To investigate the effect of andrographolide(AP)on vascular endothelial inflammation and high mobility group box 1(HMGB1)/receptor of advanced glycation end product(RAGE)signaling pathway in rats with thrombosis angiitis obliterans(TAO).Methods:A TAO rat model was established and the successfully modeled rats were randomly divided into a model group(TAO group),low-dose and high-dose andrographolide groups(AP-L and AP-H groups),and high-dose andrographolide+pathway activator group(AP-H+rHMGB1 group),with 12 rats in each group.Another 12 healthy rats served as the control group(Control group).The TAO lesions of rats in each group were graded and scored.Blood viscometer was used to measure whole blood and plasma viscosity.ELISA was utilized to detect levels of thrombotic factors.H-E staining was applied to observe the pathological morphology of femoral artery tissue.Western blotting was employed to detect the protein expression related to vascular endothelial inflammation and HMGB1/RAGE signaling pathway.Results:Compared with the Control group,the TAO group exhibited more severe shedding of endothelial cells in the femoral artery tissue,with a large amount of thrombus formation.The whole blood viscosity,plasma viscosity,thromboxane B2(TXB2)levels,and expressions of IL-6,intercellular adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),HMGB1,RAGE,and p-NF-κB p65/NF-κB p65 elevated,while the 6-Keto-prostaglandin F1α(6-Keto-PGF1α)level decreased.Compared with the TAO group,the AP-L and AP-H groups showed reduced shedding of endothelial cells and mild thrombosis in the femoral artery tissue,with decreased whole blood viscosity,plasma viscosity,TXB2 level,and IL-6,ICAM-1,VCAM-1,HMGB1,RAGE,and p-NF-κB p65/NF-κB p65 expression,and increased 6-Keto-PGF1α level.Compared with the AP-H group,the AP-H+rHMGB1 group exhibited worsened shedding of endothelial cells and increased thrombosis in femoral arterial tissue,with elevated whole blood viscosity,and plasma viscosity.The TXB2 level and and expression of IL-6,ICAM-1,VCAM-1,HMGB1,RAGE,and p-NF-κB p65/NF-κB p65 increased,while the 6-Keto-PGF1α level decreased.Conclusion:Andrographolide can alleviate vascular endothelial inflammation in TAO rats,and its mechanism may be associated with the inhibition of the HMGB1/RAGE signaling pathway.
王永红;林琳
儋州市人民医院,介入血管科,儋州 571700儋州市人民医院,骨一科,儋州 571700
医药卫生
穿心莲内酯高迁移率族蛋白1晚期糖基化终末产物受体血栓闭塞性脉管炎血管内皮炎症
andrographolidehigh mobility group box 1receptor of advanced glycation end productthrombo angiitis obliteransvascular endotheliuminflammation
《解剖学杂志》 2026 (2)
138-142,5
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