普伐他汀抑制oxLDL诱导的人外周血单核细胞CD11b表达及与内皮的粘附

目的探讨普伐他汀对氧化修饰低密度脂蛋白（ｏｘＬＤＬ）诱导的人外周血单核细胞（ＰＢＭｓ）粘附功能的影响，揭示其除调脂外的抗炎作用。方法在体外分离培养人ＰＢＭｓ和脐静脉内皮细胞（ＨＵＶＥＣ），ＰＢＭｓ经ｏｘＬＤＬ诱导后，应用流式细胞仪和β Ｎ 乙酰氨基己糖苷酶比色法，检测单核细胞粘附分子ＣＤ１１ｂ表达及对ＨＵＶＥＣ的粘附，以及普伐他汀的作用。结果普伐他汀在５０μｍｏｌ·Ｌ－１即可抑制ｏｘＬＤＬ诱导的ＰＢＭｓ对ＨＵＶＥＣ的粘附以及下调ＣＤ１１ｂ的表达（Ｐ＜００１），呈浓度依赖方式；甲羟戊酸可对抗此抑制作用。结论普伐他汀除调脂作用外，尚可抑制循环血单核 巨噬细胞至内皮粘附聚集，具有抗炎作用；其机制与普伐他汀抑制胆固醇前体物质甲羟戊酸生成有关。

Pravastatin inhibits CD 11b expression and adhesion of oxLDL induced human peripheral blood monocytes to endothelium

AIM To explore the effect of oxLDL inducing human peripheral blood monocytes in adhesion, and the anti inflammatory role except its modulating lipids. METHORDS PBMs and HUVEC were isolated and cultured in vitro . After PBMs were induced by oxLDL, the CD 11b expression and adhesion of PBMs to HUVEC were measured by flow cy tometry and β nitrophenl N acetyl β D glucosminide test, furthermore the effect of pravastatin on them was also investigated. RESULTS Pravastatin in 50 μmol·L -1 inhibited the adhesion of oxLDL inducing PBMs to HUVEC, and downregulated the expression of CD11b in dose dependent manner ( P <0 01), This effect was fully prevented by the addition of mevalonate. CONCLUTION Independence of modulating lipids, pravastatin could inhibit adhesion and aggregation of monocyte macrophages to endothelium in circulation, and may have anti inflammatory action. The mechanism in reducing development of atherosclerosis by pravastatin may be related to interfering with products of cholesterol precursor mevalonate.