摘要
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＜ ００１） ， 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＜ ００５） ，同时还可使肝细胞 Ａ Ｌ Ｔ 释放率下降，细胞活力上升（ Ｐ＜ ００５） 。结论 Ｍ Ｔ 拮抗 Ｃ Ｃｌ４
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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1999年第4期311-313,共3页
Chinese Pharmacological Bulletin
基金
安徽省自然科学基金
关键词
褪黑素
四氯化碳
抗氧化剂
肝损伤
melatonin
carbon tetrachloride
antioxidant
liver damage
