菊粉对酒精性肝病小鼠单核细胞型骨髓来源抑制性细胞的影响

Effects of Inulin on Monocytic Myeloid Derived Suppressor Cells in Alcoholic Liver Disease in Mice

目的探讨菊粉对酒精性肝病(alcoholic liver disease,ALD)防治的机制。方法将60只雌性C57BL/6J小鼠随机分为4组:阴性对照组、菊粉干预阴性对照组、ALD模型组和菊粉干预ALD模型组,每组15只。每组小鼠给予等热量Lieber-decarli(LD)液体饮食。喂养6周后,处死小鼠,流式细胞术检测外周血、肝脏和脾脏样本的单核细胞型骨髓来源抑制性细胞(M-MDSCs),流式CBA分析血浆中肿瘤坏死因子-α(TNF-α)和白细胞介素-10(IL-10)水平。并分析各组M-MDSCs比例和血清炎症因子水平的相关性。结果模型组小鼠外周血、肝脏和脾脏M-MDSCs比例高于阴性对照和菊粉干预阴性对照组;菊粉干预ALD模型组M-MDSCs在外周血、肝脏和脾脏中的比例较ALD模型组升高(P<0.05或<0.01)。菊粉干预ALD模型组较ALD模型组外周血TNF-α水平降低,IL-10水平升高(P均<0.05)。外周血、肝脏及脾脏中M-MDSCs分别与TNF-α呈负相关,与IL-10呈正相关(P均<0.05)。结论菊粉可提高酒精性肝病小鼠外周血、肝脏和脾脏M-MDSCs比例,同时降低外周血炎症细胞因子水平。

Objective To investigate the effects of inulin on prevention and treatment of alcoholic liver disease(ALD).Methods Sixty female C57BL/6J mice were randomly divided into four groups:negative control group,ALD model group,inulin-treated negative control group and inulin-treated ALD treated group,with 15 mice in each group.All mice were fed with isocaloric modified Lieber-DeCarli liquid diets.After 6 weeks of feeding,mice were euthanized and blood samples,livers and spleens were collected respectively.The proportion of M-MDSCs and levels of inflammatory indicators TNF-αand IL-10 were measured by flow cytometry.The correlations of M-MDSCs and inflammatory indicators were analyzed.Results The proportions of M-MDSCs in peripheral blood,liver and spleen in ALD group were significantly higher than those in negative control group or inulin intervention negative control group,respectively;the proportions of M-MDSCs in peripheral blood,liver and spleen in inulin-treated ALD group were also increased than that in ALD model group,respectively(P<0.01 or<0.05).The level of TNF-αin inulin-treated ALD group was lower than that in ALD model group;the level of IL-10 was higher than that in ALD model group(P<0.05).The proportion of M-MDSCs in peripheral blood,liver and spleen were negatively correlated with the level of TNF-α,and positively correlated with IL-10(P all<0.05).Conclusion Dietary inulin ameliorates ALD via increasing M-MDSCs in mice and suppressing inflammatory indicators as well.