高血压患者外周血单核细胞分泌TNF-α、IL-6水平及洛伐他汀干预研究

目的观察原发性高血压患者外周血单核细胞(PBMC)肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)分泌水平及洛伐他汀干预后TNF-α、IL-6分泌水平的变化。方法原发性高血压患者(观察组)86例,健康对照组82例,体外培养PBMC,酶联免疫吸附双抗体夹心法检测培养上清液PBMC的自发分泌、脂多糖(LPS)刺激分泌、洛伐他汀干预LPS刺激分泌TNF-α、IL-6水平,并与正常对照组比较。结果①观察组PBMC分泌TNF-α、IL-6水平高于对照组(P<0.001)。②LPS刺激后两组TNF-α、IL-6均较自发分泌时明显升高(P<0.001),与正常对照组相比,观察组LPS刺激PBMC分泌TNF-α、IL-6增加(P<0.001)。③洛伐他汀干预后,两组均明显较LPS刺激和自发分泌时的TNF-α、IL-6降低(P<0.001)。结论炎症可能参与原发性高血压的发生发展,洛伐他汀可以减轻其炎症反应。

Study on increased secretion of tumour necrosis factor alpha and interleukin-6 by peripheral blood monocytes of patients with essential hypertension induced by lovastatin

Objective To study the secretion level of TNF-α,IL-6 by PBMC and their changes in level after the intervention of lovaststin in patients with essential hypertension.Methods A total of 86 patients with essential hypertension（study group） and 82 healthy controls were included in this study.PBMC were cultured in vitro.Double antibody sandwich enzyme-linked immunosorbent assay was applied for examination of the spontaneous secretion of TNF-α and IL-6 by PBMC,secretion of TNF-α and IL-6 after exposure to LPS,and secretion of TNF-α and IL-6 after exposure to LPS and lovastatin intervention.All these findings of patients in study group were compared with those of control group.Results ①The secretion level of PBMC for TNF-α,IL-6 was higher in patients of study group than those of control group,the difference was statistically significant（P0.001）.②The secretion levels of TNF-α and IL-6 were higher in study group than those in control group after exposure to LPS（P0.001）.The secretion levels of TNF-α and IL-6 were significantly higher in two groups after exposure to LPS than the levels of spontaneous secretion of TNF-α and IL-6 by PBMC（P0.001）.③ The secretion levels of TNF-α and IL-6 were significantly decreased in two groups after lovastatin intervention（P0.001）.Conclusion These data show that inflammation may be involved in the process and development of essential hypertension,and lovastatin can reduce the inflammatory response.