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目的 :观察血管紧张素Ⅱ 1型受体 (AT1R)拮抗剂伊贝沙坦 (Irb)对脂多糖 (LPS)诱导的体外培养人脐静脉血管内皮细胞 (HUVEC)核因子 κB(NF κB)激活与肿瘤坏死因子 α(TNF α)、细胞间粘附分子 1(ICAM 1)表达的影响。方法 :体外培养的第 3～ 5代HUVEC用于实验。用免疫组织化学分析检测细胞NF κB亚单位p6 5、ICAM 1的表达程度 ,酶联免疫吸附法检测培养液上清TNF α浓度。 结果 :LPS有效激活NF κB并诱导HU VEC表达TNF α、ICAM 1增加 ;Irb预先孵育 2h能抑制NF κB并减轻LPS诱导的HUVECTNF α和ICAM 1表达。结论 :LPS可能通过激活NF κB使TNF α、ICAM 1表达增加损伤血管内皮功能 ;Irb能保护因感染而致心血管疾病中的血管内皮功能 ,至少部分通过抑制NF κB这一途径而降低血管内皮TNF α、ICAM 1表达。
OBJECTIVE: To observe the effects of Irb, an antagonist of angiotensin Ⅱ type 1 receptor (AT1R), on activation of nuclear factor κB (NF κB) induced by lipopolysaccharide (LPS) in cultured human umbilical vein endothelial cells (HUVECs) And tumor necrosis factor α (TNF α), intercellular adhesion molecule 1 (ICAM 1) expression. Methods: The 3rd to 5th passage HUVEC cultured in vitro were used in the experiment. The expression of NF-κB subunit p6 5 and ICAM 1 was detected by immunohistochemistry. The concentration of TNF-α in culture supernatant was detected by enzyme-linked immunosorbent assay. Results: LPS activated NF κB and induced the expression of TNF α in HU VEC, and increased ICAM 1. Preincubation with Irb for 2 h inhibited NF κB and LPS-induced expression of HUVECTNF α and ICAM 1. CONCLUSION: LPS may damage endothelial function by activating NF-κB and increasing the expression of TNF-α and ICAM-1. Irb can protect vascular endothelial function induced by infection and reduce vascular endothelial growth at least partly through the inhibition of NF-κB TNFα, ICAM 1 expression.