论文部分内容阅读
为探讨微量元素硒和锌在体内抗低密度脂蛋白氧化的作用及其可能机制 ,采用硫代巴比妥酸法测定大鼠动脉平滑肌细胞对低密度脂蛋白的氧化反应 ,采用噻唑蓝法了解动脉平滑肌细胞增殖及邻联二茴香胺底物反应的方法测髓过氧化物酶活性。结果表明 10 μmol/L亚硒酸钠显著减少了丙二醛的生成 ,而相同浓度的硫酸锌效应不明显 ,但二者均可见动脉平滑肌细胞增殖减少。此外 ,低密度脂蛋白诱导动脉平滑肌细胞的髓过氧化物酶活性显著升高 ,但 10 μmol/L亚硒酸钠似乎不能抑制这种效应。提示硒与锌均抑制氧化型低密度脂蛋白促动脉平滑肌细胞的增殖作用 ,前者与抗低密度脂蛋白氧化有关 ,且可能发生在髓过氧化物酶催化形成酪酰基自由基之后的某个环节 ,后者尚待进一步探讨。
To investigate the effect of trace element selenium and zinc on the oxidation of low density lipoprotein in vivo and its possible mechanism, the oxidative reaction of rat arterial smooth muscle cells to low density lipoprotein was measured by thiobarbituric acid method. The thiazolyl blue method was used to understand Arterial smooth muscle cell proliferation and o-dianisidine substrate reaction method measured myeloperoxidase activity. The results showed that 10 μmol / L sodium selenite significantly reduced the formation of malondialdehyde, but the same concentration of zinc sulfate was not obvious, but both showed reduced proliferation of arterial smooth muscle cells. In addition, low density lipoprotein induced a marked increase in myeloperoxidase activity in arterial smooth muscle cells, but sodium selenite at 10 μmol / L did not appear to suppress this effect. It is suggested that both selenium and zinc inhibit the proliferation of arterial smooth muscle cells induced by oxidized low-density lipoprotein. The former is related to the oxidation of anti-LDL and may occur somewhere after myeloperoxidase catalyzes the formation of pivaloyl free radical , The latter needs to be further explored.