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本工作观察了神经降压素（ＮＴ）对醋氨酚引起的小鼠在体肝脏和高体肝细胞损伤的保护作用及其与各胱甘肽系统的关系。结果表明，ＮＴ在整体和离体肝细胞均能减轻醋氨酚诱导的转氨酶的漏出，且在离体肝细胞部分翻转了醋氨酚引起的ＤＮＡ合成速率的下降。在离体肝细胞醋氨酚使细胞内还原型谷胱甘肽（ＧＳＨ），谷胱甘肽总含量和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均降低，但氧化型谷胱甘肽（ＧＳＳＧ）含量无明显改变。ＮＴ预处理后再给予酪氨酚，则ＧＳＨ含量进一步下降，而ＧＳＳＧ、谷胱甘肽总含量及ＧＳＨ－ＰＸ活性均增加，提示ＮＴ一方面促进谷胱甘肽的合成，另一方面通过提高ＧＳＨ－Ｐｘ的活性，促进ＧＳＨ转变成ＧＳＳＧ，从而提高了肝细胞清除自由基的功能。
This work observed the neurotensin (NT) on acetaminophen-induced mouse liver injury in vivo and hepatocytes damage and its relationship with the role of each glutathione system. The results showed that NT attenuated acetaminophen-induced transaminase leakage in both intact and ex vivo hepatocytes and decreased DNA synthesis rate induced by acetaminophen in partially isolated hepatocytes. Acetaminophen in isolated hepatocytes decreased the contents of GSH, GSH-Px and GSH-Px, but the activity of oxidized glutathione Glycopeptide (GSSG) content did not change significantly. NT pretreatment followed by the addition of tebufenozide, the GSH content further decreased, while the GSSG, total glutathione content and GSH-PX activity were increased, suggesting NT on the one hand to promote glutathione synthesis, on the other hand by increasing GSH-Px activity, promote the GSH into GSSG, thereby enhancing the function of liver cells to scavenge free radicals.