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目的 研究2,3,7,8-四氯二苯并二(恶)英(2,3,7,8-TCDD)引起大鼠肝脏发生脂肪变性的作用机制.方法 将16只健康成年SPF级雄性SD大鼠随机分为2组,分别为(玉米油)对照组和2,3,7,8-TCDD染毒组,每组8只.首次以6.4 μg/kg剂量进行腹腔注射染毒,后每隔1周以首次剂量的21％(1.344 μg/kg)进行染毒,染毒容量为10 ml/kg,连续3周.于首次染毒后4周末,测定血清和肝脏中甘油三酯含量,采用RT-PCR法检测肝脏脂肪合成相关酶乙酰辅酶A羧化酶1(ACC1)、脂肪酸合成酶(FAS)、硬脂酰辅酶A去饱和酶1(SCD1)mRNA的表达水平.结果 与对照组比较,2,3,7,8-TCDD染毒组大鼠肝脏中的甘油三酯含量较高,差异有统计学意义(P＜0.05);而血清中的甘油三酯含量无明显改变.与对照组比较,2,3,7,8-TCDD染毒组大鼠肝组织中ACC1、FAS mRNA的表达水平均较高,差异有统计学意义(P＜0.05);而SCD1 mRNA的表达水平无明显改变.结论 2,3,7,8-TCDD可通过上调肝组织ACC1、FAS mRNA的表达水平,来干扰肝脏脂质合成代谢,造成肝脏脂质沉积.“,”Objective To investigate the mechanism of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced steatosis in rat liver.Methods A total of 16 health SPF level SD rats were randomly divided into two groups (eight in each group),namely the control and 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure groups.The first dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin was 6.4 μg/kg body weight,thereafter,a maintenance dosage by 21％ of the first dose(1.344 μg/kg) weekly for three weeks,and treatments were conducted with capacity of 10 ml/kg body weight by intraperitoneal injection.Four weeks after the first expourse,triglyceride levels in serum and liver were detected,and acetyl-CoA carboxylase(ACC1),fatty acid synthetase(FAS),stearoyl-CoA desaturase1 (SCD1) genes relative expression levels in liver were detected by using real time-PCR.Results Compared with the control group,triglyceride in liver was higher in 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure group(P＜0.05).There was no significant difference in serum triglyceride between control group and 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure group.Compared with the control group,A CC1 and FAS mRNA expression level were higher in 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure group (P＜0.05).There was no significant difference in SCD1 mRNA expression level between control group and 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure group.Conclusion 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure may cause lipid deposition and interfere lipid synthesis in liver through up-regulating A CC1 and FAS mRNA expression levels.