刺梨利康饮对慢性汞中毒脂质过氧化损害的拮抗作用

Antagonistic Effects of Rosa Roxburghii Tratt Likangyin on Lipid Peroxidation Injuries Induced by Chronic Mercury Poisoning

用８３７－４９μｍｏｌ／Ｌ 含汞水饲养大鼠８ 周，复制出慢性汞中毒模型，然后分别自由饮用含维生素Ｃ６８１２－７６μｍｏｌ／Ｌ 的利康饮和ｉｐ １２５ｍｇ／ｋｇ 二巯基丙磺酸钠（ＤＭＰＳ）３ 周，探讨利康饮和ＤＭＰＳ 对慢性汞中毒大鼠尿汞排泄和脂质过氧化损害的影响。结果发现，慢性汞中毒引起血清、肝、脑和肾还原型谷胱甘肽（ＧＳＨ） 含量显著降低，血清、肝、脑和肾丙二醛（ ＭＤＡ） 含量、尿蛋白含量及尿碱性磷酸酶（ＡＫＰ） 活性显著升高；利康饮可显著增加尿汞排泄和血清维生素Ｃ 含量，并使慢性汞中毒引起的血清、肝、脑和肾ＧＳＨ 含量显著回升，血清、脑和肾ＭＤＡ 含量、尿蛋白含量及尿ＡＫＰ 活性显著回降；ＤＭＰＳ 虽有明显促进尿汞排泄效果和使血清ＭＤＡ 含量显著回降的作用，但对慢性汞中毒引起的其它脂质过氧化损害指标影响不明显。结果表明，刺梨利康饮具有一定排汞效果，并对慢性汞中毒引起的机体抗氧化功能降低和脂质过氧化损害具有明显拮抗作用。

In order to know the effects of Likangyin and sodium dimercato propane sulfanate(DMPS)on the excretion of urine mercury and the lipid peroxidation injuries induced by chronic mercury poisoning in rats,we made chronic mercury poisoning model by feeding rats with the drinking containing mercury 837 49μmol/L for 8 weeks.Then mercury intoxicated rats drank freely the likangyin containing vitamin C(Vit C)6812 76μmol/L and were given intraperitoneally 125 mg/Kg DMPS for 3 weeks respectively.The following results were obtained:The glutathion(GSH)contents of serum,liver,brain and kidney were decreased significantly and the malondialdehyde(MDA)contents of serum,liver,brain and kidney and the protein contents and the alkaline phosphatase(AKP) activities of urine were increased markedly by chronic mercury poisoning.Likangyin could raise significatly the excretion of urine mercury and the Vit C contents of serum.The significant increases of GSH contents in serum,liver,brain and kidney and the significant decreases of MDA contents in serum,brain and kidney and protein contents and AKP activities in urine were induced by Likangyin in mercury intoxicated chronically rats.DMPS was effective in elimianting urine mercury and in lowering MDA contents of serum,but it has no effects on the other indices of lipid peroxidation injuries induced by chronic mercury poielminating.The results suggested that Likangyin was effective in eliminating mercury and markedly antagonized the decreases of body’s antioxidate effects and the lipid peroxidation injuries induced by chronic mercury poisoning.