Glycine accelerates recovery from alcohol-induced liver injury.
Glycine accelerates recovery from alcohol-induced liver injury.
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发表时间：
1998-08
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通讯作者：
M. Yin;K. Ikejima;G. Arteel;V. Seabra;B. Bradford;H. Kono;I. Rusyn;R. G. Thurman
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作者：
M. Yin;K. Ikejima;G. Arteel;V. Seabra;B. Bradford;H. Kono;I. Rusyn;R. G. Thurman
甘氨酸可预防缺氧-复氧引起的肝脏损伤，减少内毒素引起的死亡率，并通过减少血液中的乙醇将酒精性肝损伤降至最低。我们的目的是研究饮食甘氨酸在酒精诱导的早期损伤恢复过程中的作用，使用一个模拟酒精患者的临床表现和组织病理学的模型。雄性Wistar大鼠连续灌胃酒精6wk，出现典型的酒精性肝损伤组织学改变，包括脂肪变性、炎症、坏死，血清天冬氨酸氨基转移酶和丙氨酸氨基转移酶水平升高。停止酒精后，一组大鼠接受对照饲料，另一组大鼠接受含甘氨酸的饲料2wk。在此期间，所研究的所有参数都趋向于回到基准值。然而，饲喂甘氨酸的大鼠血清天冬氨酸氨基转移酶和丙氨酸氨基转移酶恢复快约30%。此外，甘氨酸组的肝脏病理评分也显著低于对照组(0.5比2.6)。1wk后，甘氨酸组(5.6%)的脂肪变性显著低于对照组(8.9%)。甘氨酸对浸润性白细胞和坏死性细胞数量的减少也明显高于对照组。甘氨酸的这种有益作用可能部分是由于甘氨酸增加了氯化物进入库普弗细胞的数量，导致肿瘤坏死因子-α的产生减少。这些结果表明，含甘氨酸的饮食加速了酒精性肝损伤的恢复过程，并可能导致其在酒精性肝炎中的临床应用。
Glycine prevents hepatic damage caused by hypoxia-reoxygenation, diminishes mortality due to endotoxin and minimizes alcoholic liver injury by decreasing blood ethanol. Our purpose was to investigate the effect of dietary glycine during recovery from early alcohol-induced injury, using a model that mimics the clinical presentation and histopathology with alcoholics. Male Wistar rats were exposed to ethanol continuously for 6 wk via intragastric feeding that resulted in typical histology of alcoholic liver injury, including steatosis, inflammation, necrosis and increased serum levels of aspartate aminotransferase and alanine aminotransferase. After cessation of ethanol, one group of rats received a control diet, the other a glycine-containing diet for 2 wk. During this period, all parameters studied tended to return to baseline values. However, serum aspartate aminotransferase and alanine aminotransferase recovered about 30% more rapidly in rats fed glycine. Further, the hepatic pathology score was also significantly lower in the glycine group than in controls (0.5 vs. 2.6). After 1 wk, steatosis was reduced significantly more in the glycine group (5. 6%) than in controls (8.9%). Glycine also diminished numbers of infiltrating leukocytes and necrotic cells significantly more than in controls. This beneficial effect of glycine may be partly explained by the fact that glycine increased influx of chloride into Kupffer cells leading to diminished tumor necrosis factor-alpha production. These results indicate that a glycine containing diet expedites the process of recovery from ethanol-induced liver injury and may lead to its clinical application in alcoholic hepatitis.