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目的通过对变异型心绞痛患者及健康对照者外周血的单核细胞给予一定浓度的C反应蛋白(CRP)的刺激,比较两组中肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)的差异,并观察他汀类药物干预后其水平的变化,探讨炎症相关分子机制在变异型心绞痛中的作用和他汀类药物的干预效应。方法培养变异型心绞痛患者(病例组,n=6)和健康对照者(对照组,n=6)的外周血单核细胞,使用CRP(终浓度为20mg/L)刺激24小时;辛伐他汀干预采用辛伐他汀(终浓度10umol/L)预先孵育单核细胞2小时,继之以CRP刺激24小时。采用酶联免疫吸附法测定培养液上清中的TNF-α和IL-6的水平,比较两组之间的差异。结果基础状态下病例组中TNF-α和IL-6的水平与对照组相比无显著差别,给予CRP刺激后,病例组及对照组中TNF-α和IL-6的水平较其基础状态均有明显升高(p<0.01),但病例组中TNF-α和IL-6的升高幅度较对照组更为显著(p<0.01),辛伐他汀预孵育后可以有效抑制两组患者CRP刺激后的TNF-α和IL-6表达(p<0.01)。结论变异型心绞痛患者受到CRP刺激后外周血单核细胞中TNF-α,IL-6的水平明显高于对照组,提示炎症机制可能在变异型心绞痛中起着一定的作用;辛伐他汀可以有效抑制变异型心绞痛患者中炎症反应的强度。
Objective To investigate the effects of C-reactive protein (CRP) on peripheral blood mononuclear cells (PBMCs) of patients with variant angina and healthy controls. The levels of tumor necrosis factor-α (TNF-α) and interleukin- (IL-6), and to observe the level of statins after intervention, to explore the role of inflammation-related molecular mechanisms in variant angina and statin intervention. Methods Peripheral blood mononuclear cells from patients with variant angina (n = 6) and healthy controls (n = 6) were cultured with CRP (final concentration 20 mg / L) for 24 hours. Simvastatin Monocytes were pre-incubated with simvastatin (final concentration 10 μmol / L) for 2 hours followed by CRP for 24 hours. The levels of TNF-α and IL-6 in the culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA), and the differences between the two groups were compared. Results The levels of TNF-α and IL-6 in the case group were not significantly different from those in the control group. The levels of TNF-α and IL-6 in the case group and the control group were significantly higher than those in the control group (P <0.01). However, the increase of TNF-α and IL-6 in case group was more significant than that in control group (p <0.01). After pre-incubation with simvastatin, CRP TNF-α and IL-6 expression after stimulation (p <0.01). Conclusion The levels of TNF-α and IL-6 in peripheral blood mononuclear cells of patients with variant angina after CRP stimulation are significantly higher than those of control group, suggesting that inflammatory mechanism may play a role in variant angina pectoris. Simvastatin can be effective Inhibit the intensity of inflammatory response in patients with variant angina.