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目的:通过观察注射用血栓通(主要成分为三七总皂苷)对各种刺激处理因素下白细胞黏附能力和黏附分子表达的影响,探讨血栓通对缺血-再灌注损伤的保护机制。方法:分离纯化大鼠白细胞与肺部血管内皮细胞,建立体外白细胞与血管内皮细胞黏附试验体系,在施加内毒素、肿瘤坏死因子(TNF-α)、白细胞介素-8(IL-8)与缺氧等刺激处理因素之前,采用血栓通(三七总皂苷剂量分别为5,50,100 mg.L-1)进行分组干预,并检测白细胞对血管内皮细胞的黏附率,同时采用流式细胞术检测白细胞黏附分子LFA-1,VLA-4与血管内皮细胞黏附分子ICAM-1,VCAM-1表达的变化。结果:在内毒素作用条件下,血栓通对大鼠白细胞黏附率无显著改变,而在TNF-α与IL-8活化因素以及缺氧条件下,50,100 mg.L-1血栓通可明显减少大鼠白细胞对内皮细胞的黏附率;在缺氧、TNF-α等刺激因素的作用下,大鼠肺血管内皮细胞VCAM-1与ICAM-1的表达水平显著升高,在100 mg.L-1血栓通的干预作用下,VCAM-1与ICAM-1的表达水平显著降低。结论:血栓通可抑制大鼠肺血管内皮细胞VCAM-1与ICAM-1的表达而降低白细胞的黏附能力,从而减轻血管内皮细胞的损伤,可能是血栓通对缺血-再灌注损伤具有保护作用的机制之一。
OBJECTIVE: To observe the effect of Xuesaitong injection (the main component of Panax notoginseng saponins) on leukocyte adhesion and expression of adhesion molecules under various stimulus factors and to explore the protective mechanism of Xueshuantong on ischemia-reperfusion injury. Methods: The leukocyte and pulmonary vascular endothelial cells were isolated and purified to establish the leukocyte and vascular endothelial cell adhesion assay system. The effects of endotoxin, tumor necrosis factor (TNF-α), interleukin-8 (IL-8) Before thrombolysis treatment, hypoxia and other stimuli were treated by Xueshuantong (Panax notoginseng saponins at doses of 5, 50, and 100 mg.L-1, respectively), and the adhesion rate of leukocytes to vascular endothelial cells was detected. Flow cytometry Changes of Leucocyte Adhesion Molecule LFA-1, VLA-4 and Vascular Endothelial Cell Adhesion Molecules ICAM-1, VCAM-1 Expression. Results: Under the action of endotoxin, there was no significant change in the adhesion rate of Xueshuantong to rats. However, 50,100 mg.L-1 of Xueshuantong obviously decreased when TNF-α and IL-8 were activated and hypoxia The adhesion rate of rat white blood cells to endothelial cells was significantly increased under hypoxia and TNF-α stimulation. The levels of VCAM-1 and ICAM-1 in rat pulmonary vascular endothelial cells were significantly increased at 100 mg.L-1 Under the intervention of Xuesaitong, the expression levels of VCAM-1 and ICAM-1 were significantly decreased. Conclusion: Xueshuantong can inhibit the expression of VCAM-1 and ICAM-1 in pulmonary vascular endothelial cells of rats and reduce the adhesion of leukocytes, thus reducing the damage of vascular endothelial cells. It may be that Xueshuantong has a protective effect on ischemia-reperfusion injury One of the mechanisms.