【摘要】 目的 观察3,3’-二吲哚甲烷(3,3’-diindolylmethane, DIM)对Lieber-DeCarli标准型(regular型)酒精液体乙醇饲料(LD饲料)诱导的小鼠酒精性脂肪肝的改善作用，并对其分子作用机制进行初步探讨。方法 将40只6～8周龄雄性C57BL/6J小鼠随机分为4组：正常对照组、酒精组、DIM(50 mg/kg)组和酒精+DIM(50 mg/kg)组，实验结束后称重，处死小鼠，收集血液和肝脏组织，分离血清测定肝功能指标，油红O染色观察肝脏的脂肪蓄积，Western blot检测内质网应激通路蛋白的表达。结果 与对照组相比，DIM对肝脏没有显著的影响，四组之间体重无显著变化。与酒精组相比，DIM处理组血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)水平显著降低(P<0.05),油红O染色和甘油三酯测定显示肝脏甘油三酯含量显著降低(P<0.05)。DIM明显减轻肝脏脂肪变性，Western blot结果表明DIM能够抑制酒精诱导的内质网通路的关键蛋白PERP、eIF和CHOP的激活作用。结论 DIM对小鼠酒精性脂肪肝具有一定的保护作用，其机制可能与抑制酒精激活的内质网应激通路有关。更多还原

【Abstract】 Objective To observe the effect of 3,3’-diindolylmethane(DIM) on improving the alcoholic fatty liver of mice induced by Lieber-DeCarli standard(regular type) alcoholic liquid ethanol feed(LD feed) and preliminarily discuss its molecular mechanism of action. Methods 40 male C57 BL/6 J mice aged 6-8 weeks were randomly divided into 4 groups: normal control group, alcohol group, DIM(50 mg/kg) group and alcohol + DIM(50 mg/kg) group. After the experiment, the mice were weighed and then killed, and their blood and liver tissues were collected; serum were separated to determine the liver function indexes, and liver tissue were stained with oil red O to observe the fat accumulation in liver; Western blot was employed to detect the protein expression of endoplasmic reticulum stress pathways. Results Compared with the normal control group, DIM had no significant effect on the liver, and there was no significant change in body weight among the four groups. Compared with the alcohol group, the levels of alanine transferase(ALT) and aspartate transferase(AST) in the serum of DIM group were significantly decreased(P<0.05), and oil red O staining and triglyceride determination showed that the content of liver triglyceride was decreased significantly(P<0.05). DIM significantly reduced the hepatic steatosis. Western blot results showed that DIM could inhibit the alcohol-induced activation of key proteins PERP, eIF and CHOP in the endoplasmic reticulum pathways. Conclusion DIM has a certain protective effect on the alcoholic fatty liver in mice, and its mechanism may be related to the inhibition of alcohol-activated endoplasmic reticulum stress pathways.更多还原