虎杖苷抑制ox-LDL诱导的脂质过氧化并下调巨噬细胞清道夫受体CD36表达

Polydatin inhibits lipid peroxidation induced by ox-LDL and down-regulates CD36 expression in macrophages

目的:研究虎杖苷抑制ox-LDL诱导的巨噬细胞氧化反应和调节巨噬细胞清道夫受体CD36表达的功效。方法:将C57/BL6小鼠随机分为生理盐水组、虎杖苷组,分别经腹腔给予1.5%生理盐水、1.5%虎杖苷溶液,连续3d,第4d停止注射,第5d处死老鼠,取腹腔巨噬细胞培养。将培养的巨噬细胞给予氧化修饰的低密度脂蛋白(ox-LDL)刺激,观察腹腔巨噬细胞超氧化物歧化酶(SOD)的活性,ox-LDL诱导的巨噬细胞呼吸爆发及脂质过氧化物(LPO)含量,以及清道夫受体CD36的表达调控。结果:与生理盐水组相比,虎杖苷组巨噬细胞的SOD活性明显提高,巨噬细胞的LPO蓄积也明显降低;并且虎杖苷组ox-LDL诱导的巨噬细胞呼吸爆发水平也显著低于生理盐水对照组;虎杖苷组巨噬细胞CD36的表达同样明显低于生理盐水组。结论:虎杖苷可有效抑制巨噬细胞脂质过氧化应激情况下的呼吸爆发,下调其清道夫受体CD36的表达,提示虎杖苷可能具有预防动脉粥样硬化早期病变的功能。

AIM： To investigate the inhibitory effect of polydatin on the reaction of oxidation and regulation of CD 36 expression in mouse macrophages. METHODS： C57/BL6 mice were divided into two groups and injected with normal saline or 1.5% polydatin （0. 2 mL/d） for 3 days. On the 5th d after the first injection, the mice were sacrificed and abdominal macrophages were collected. The activity of superoxide dismutase （ SOD）, the levels of oxidative burst and lipid peroxide （LPO）, and the expression of CD36 in the cells were assayed. RESULTS： In polydatin group, SOD activity in the macrophages was higher, the oxidized low density lipoprotein （ ox - LDL） induced macrophage respiratory burst level and the accumulation of lipid peroxide （LPO） were significantly lower than those in PBS control group. Polydatin also prevented ox - LDL - induced expression of scavenger receptor CD36 on the macrophages. CONCLUSION： Polydatin enhances the anti - oxidant ability in macrophages by inhibiting the mitochondrial oxidative burst and expression of scavenger receptor CD36, indicating that polydatin is an appropriate reagent for anti - aging and anti - atherosclerosis.