褪黑素对四氯化碳小鼠肝损伤的保护作用

目的　探讨褪黑素对四氯化碳肝毒性的保护作用。方法　给予小鼠四氯化碳（５ ｍｌ·ｋｇ － １ ） ，继后每隔６ ｈ ｉｐ 褪黑素１０ ｍ ｇ·ｋｇ － １ 。用胶原酶消化法分离小鼠肝细胞后，依次加用褪黑素（１０ － ５ ～１０ － １ １ ｍｏｌ· Ｌ－ １ ） 和四氯化碳（２０ ｍ ｍ ｏｌ· Ｌ－ １ ） 。以测定丙氨酸氨基转换酶（ Ａ Ｌ Ｔ） ，丙二醛（ Ｍ Ｄ Ａ） 和谷胱甘肽过氧化物酶活力，作为四氯化碳肝损伤的指标。用 Ｍ Ｔ Ｔ 法检测肝细胞活力。结果　四氯化碳可使小鼠血液 Ａ Ｌ Ｔ 活性和肝 Ｍ Ｄ Ａ 含量明显上升。体内应用 Ｍ Ｔ １０ ｍ ｇ·ｋｇ － １ ，则明显降低肝匀浆 Ｍ Ｄ Ａ 含量（ Ｐ＜ ００１） ， 对血浆 Ａ Ｌ Ｔ 活性无明显影响。体外应用 Ｍ Ｔ（１０ － ５ ～１０ － ７ ｍｏｌ· Ｌ－ １ ） 亦可使肝细胞 Ｍ Ｄ Ａ 含量下降（ Ｐ＜ ００５） ，同时还可使肝细胞 Ａ Ｌ Ｔ 释放率下降，细胞活力上升（ Ｐ＜ ００５） 。结论　 Ｍ Ｔ 拮抗 Ｃ Ｃｌ４ 肝毒性的作用可能与其抗氧化能力有关

Protective effect of melatonin on carbon tetrachloride induced oxidative liver damage in mice

AIM To investigate the protective effect of melatonin (MT) on carbon tetrachloride (CCl 4) induced liver damage in mice. METHODS Mice were treated with MT(10 mg·kg -1 ) at interval of 6 hours after administration of CCl 4(5 ml·kg -1 , ip). The preparation of mouse liver cells was performed by collagenase Ⅵ perfusion, and then the hopats was incubated with CCl 4 in the presence and absence of MT(10 -5 ～10 -11 mol·L -1 ). The content of malonaldehyde (MDA)、 alanine aminotransferase (ALT) and glutathione peroxidase (GSH px) activity were assayed as indications of CCl 4 induced liver damage. Cell viability was measured by means of MTT method. RESULTS CCl 4 induced significantly high levels of plasma ALT and liver MDA in mice. CCl 4 induced MDA production in the liver was inhibited by MT treatment, but the elevated level of ALT was not reduced in mice. In in vitro study, MT prevented CCl 4 produced ALT release and MDA formation from hepatocytes in a concentration dependent manner(10 -5 ～10 -7 mol·L -1 ), and improved the cell viability ( P <0 05). CONCLUSION MT confers protection against the deterious effect of CCl 4 to mice liver, possibly due to its antioxidative capability.