摘要目的 观察在肥胖导致的非酒精性脂肪性肝病的进展过程中系统免疫及肠道免疫屏障的变化.方法 90只雄性SD大鼠均分为3组,即为正常饮食组、高糖饮食组、高脂饮食组,建立非酒精性脂肪性肝病大鼠模型,并于4、8、12周各组分别处死10只.肝脏HE染色观察肝脏脂肪变程度.鲎试验终点显色法检测门静脉血中内毒素水平.流式细胞术检测外周血单个核细胞及小肠集合淋巴结(PP结)中淋巴细胞CD4-CD8比值.结果 高糖饮食组在所有时间点内毒素水平均无显著升高,与正常饮食组差异均无统计学意义(P值均＞0.05).而高脂饮食组在8周时内毒素水平显著上升,与正常饮食组差异有统计学意义(P＜0.05).高糖饮食组与高脂饮食组在4周时外周血单个核细胞CD4/CD8显著高于正常饮食组(P值均＜0.05),至8周、12周时均显著低于正常饮食组(P值均＜0.05).PP结中CD4/CD8,高糖饮食组与高脂饮食组4、8周与外周血单个核细胞CD4/CD8变化趋势一致,12周时CD4/CD8与正常饮食组差异无统计学意义(P值均＞0.05).结论 肥胖可以抑制系统免疫及肠道免疫,肝脏可能参与调节肠道免疫.

abstractsObjective To study the changes of system immune and intestinal immune in the progression of non-alcoholic fatty liver disease due to obesity. Methods Ninty male SD rats were divided into control, high-sucrose and high-fat diet groups. Non-alcoholic fatty liver disease models were established by feeding with high-sucrose diet or high-fat diet and were killed at the 4th,8th and 12th weeks with 10 each for each group. The extent of liver steatosis was observed with HE staining.Portal blood endotoxin level was assessed by limulus test. The percentage of CD4+ and CD8+ cells in peripheral blood mononuclear cells (PBMC) and lymphocytes in Peyer's patches (PP) were calculated by flowcytometry. Results In comparison with control group, the endotoxin level was not elevated from the 4th week to 12th week in high-sucrose diet group, (all P values＞0.05), but was increased in high-fat diet group at the 8th week (P＜0.05). CD4/CD8 ratio in PBMC was higher in high-sucrose and higt-fat diet groups than that in control group at the 4th week (P＜0. 05) ,but was lower than that in control group at the 8th and 12th weeks (P＜0. 05). Whereas the variation of CD4/CD8 ratio in PP was consisted with that in PBMC between the high-sucrose and high-fat diet groups at the 4 th and 8 th weeks, but there was no difference when compared with control group at the 12 th week (P＞0.05).Conclusion Obesity can inhibit systematic immune and intestinal immune. The intestinal immune may be regulated by the liver.