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目的 研究山莨菪碱（Ａｎｉ）在红细胞自氧化损伤中的作用。方法 在红细胞悬液中加入不同浓度Ａｎｉ，温育２４ｈ，分别用比色法、硫代巴比妥酸荧光法、荧光偏振法测定红细胞溶血度、红细胞膜脂质过氧化物（ＬＰＯ） 、红细胞膜微粘度。结果 Ａｎｉ１－０，１－５ ｍ ｍｏｌ·Ｌ－１ 可显著抑制红细胞自氧化溶血（ 溶血度分别为：０－５８５ ±０－０２８、０－４３９ ±０－０２４，对照组为０－７９８ ±０－０３５ ，Ｐ＜０－０１）、显著降低红细胞膜ＬＰＯ〔分别为：（０－３５９ ±０－０１７） 、（０－３２３ ±０－０１９）μｍｏｌ·ｇ－１ Ｐｒｏ，对照组为（０－４１８±０－０１５）μｍｏｌ·ｇ－１ Ｐｒｏ， Ｐ＜ ０－０１〕、显著降低红细胞膜微粘度〔分别为：（０－３２８±０－０１７）、（０－２９６ ±０－０１９）Ｐａ·ｓ，对照组为（０－３７４ ±０－０１４） Ｐａ·ｓ〕。结论 Ａｎｉ 抗氧自由基引发的膜脂质过氧化、保护细胞膜，对红细胞自氧化损伤有保护作用
Objective To study the role of Ani in erythrocyte autooxidation injury. Methods Different concentrations of Ani were added to the erythrocyte suspensions and incubated for 24 h. The hemolysis, erythrocyte membrane lipid peroxides (LPO), erythrocytes and erythrocytes were determined by colorimetry, thiobarbituric acid fluorescence and fluorescence polarization respectively. Membrane micro-viscosity. Results Ani1-0,1-5 m mol·L-1 could significantly inhibit erythrocyte auto-hemolysis (hemolysis were 0-585 ± 0-028, 0-439 ± 0-024, 0-798 ± (0-0359 ± 0-017), (0-323 ± 0-019) μmol · g-1 Pro, while the control group was (0-035, P <0.01) 0-418 ± 0-015) μmol · g-1 Pro, P <0-01〕, significantly reduced the microviscosity of erythrocyte membrane [(0-328 ± 0-017), (0-296 ± 0-019 ) Pa · s in the control group and (0-374 ± 0-014) Pa · s〕 in the control group. Conclusions Antioxidant free radical-induced membrane lipid peroxidation protects the cell membrane and protects erythrocyte auto-oxidative damage