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作 者:李玉洁[1] 李元建[1] 吴晋湘 余先杰[1] 严幼芳[1]
机构地区:[1]湖南医科大学药理教研室
出 处:《中国药理学报》1994年第5期407-410,共4页Acta Pharmacologica Sinica
基 金:Project supported by the National Natural Science Foundation of China,№ 3880737.
摘 要:观察了四甲基吡嗪(TMP)对LDL损伤内皮细胞(EC)的保护作用。LDL(1.5 mgprotein·ml^(-1))显著增高EC的MDA含量,抑制SOD活性,降低cGMP和epoprostenol含量。LDL的毒性作用可被TMP(20mg和150mg·L^(-1)所消除。结果提示,TMP可通过促进epoprostenol的生成和/或释放保护EC。ABSTRACT Effects of tetramethylpyrazine (TMP) on endothelial cells damaged by low-density lipoproteins (LDL) were investigated. When endothelial cells were incubated with LDL (1. 5 mg protein·ml-1) the level of mal-ondialdehyde (MDA) was increased and the activity of superoxide dismutase (SOD) was inhibited, and levels of cGMP and epoprostenol were decreased. TMP at concentrations of both 20 and 150 mg·L-1 nullified the inhibition of SOD activity and the reduction of cGMP and epoprostenol content elicited by LDL. However, the elevation of MDA content induced by LDL was negated by TMP only at 150 mg·L-1. TMP also caused a reduction in MDA content and an increase of epoprostenol level in normal endothelial cells. This study suggests that TMP protects en- and that the protection of TMP might be due to reduction in lipid peroxidation through stimulation of production and / or release of epoprostenol.
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