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目的探讨甘氨酸(Gly)对内毒素(LPS)性肝损害的保护机制。方法BABL／c小鼠随机分为两组,LPS组经腹腔注射10 mg／kg的LPS,Gly组在注射相同剂量LPS前3 d开始喂饲含5％Gly的饲料。光镜观察组织病理学改变、免疫组织化学法检测Toll样受体4(TLR4)表达水平；酶联免疫吸附法检测血浆肿瘤坏死因子(TNF)α、白细胞介素10(IL-10)浓度及逆转录聚合酶链反应检测肝组织中TNFα、IL-10及TLR4的mRNA表达水平。结果Gly能明显提高小鼠存活率,肝脏病理损害程度减轻；Gly组TNFα水平显著低于LPS组,差异有统计学意义[(1852.80±126.64)pg／ml对(708.83±51.29)pg／ml,P＜0.05]；Gly组IL-10增加且高峰前移,与LPS组比较差异有统计学意义[(418.64±38.86)pg／ml对(344.09±31.70)pg／ml,P＜0.05]；Gly组肝组织中TNFα及TLR4表达也明显减弱,IL-10表达明显增强,与LPS组比较差异均有统计学意义[分别为TNFα：A值1.59±0.14对0.91±0.11；TLR4：A值0.97±0.12对0.53±0.11；IL-10：A值0.62±0.08对1.06±0.15；P值均＜0.05]。结论Gly能明显减轻LPS所致的肝损害,其机制可能与其下调肝脏各种细胞的TLR4表达,同时上调IL-10的水平有关。
Objective To investigate the protective mechanism of glycine on endotoxin (LPS) -induced liver damage. Methods BABL / c mice were randomly divided into two groups: LPS group was injected intraperitoneally with 10 mg / kg LPS, and Gly group was fed with 5% Gly 3 days before injection of the same dose of LPS. The changes of histopathology were observed with light microscope. The expression of TLR4 was detected by immunohistochemical method. The levels of plasma tumor necrosis factor (TNF) α, interleukin 10 (IL-10) Reverse transcriptase polymerase chain reaction was used to detect the mRNA expression of TNFα, IL-10 and TLR4 in liver tissue. Results Gly could significantly improve the survival rate of mice and alleviate the degree of hepatic pathological damage. The level of TNFα in Gly group was significantly lower than that of LPS group [(1852.80 ± 126.64) pg / ml vs (708.83 ± 51.29) pg / ml, (P <0.05). Compared with LPS group, the level of IL-10 in Gly group increased and peaked earlier than that in LPS group [(418.64 ± 38.86) pg / ml vs 344.09 ± 31.70 pg / ml, P <0.05] Compared with LPS group, the expression of TNFα and TLR4 were significantly decreased and the expression of IL-10 was significantly increased in group [the TNFα: A value was 1.59 ± 0.14 vs 0.91 ± 0.11; TLR4: A value was 0.97 ± 0.12 vs 0.53 ± 0.11; IL-10: A values were 0.62 ± 0.08 vs 1.06 ± 0.15; P values were all <0.05]. Conclusion Gly can significantly reduce the hepatic damage induced by LPS, and its mechanism may be related to its down-regulation of TLR4 expression in various liver cells and up-regulation of IL-10 level.