【摘要】 目的探讨一次性支气管内给予黄曲霉毒素G1(AFG1)对大鼠肺组织的影响。方法经支气管一次性给予30μg.kg-1AFG1处理雄性SD大鼠。AFG1处理1,3,7和14 d后,分别处死实验动物,以扫描电镜方法观察大鼠肺组织超微结构变化,采用原位杂交方法检测肺组织肿瘤坏死因子-α(TNFα-)mRNA表达情况,测定H2O2的降低量代表抗氧化能力。结果溶剂对照组肺组织超微结构、TNFα-mRNA表达和抗氧化能力和对照组比较未见明显改变。AFG1处理后,扫描电镜观察可见肺泡壁增厚且粗细不均,肺泡腔表面细胞有隆起,细胞肿胀,Ⅱ型肺泡上皮细胞表面微绒毛变短、消失,病变以AFG1处理后7和14 d为明显。原位杂交法结果表明,AFG1处理后1,3,7和14 d组肺组织肺泡细胞TNF-αmRNA表达的阳性细胞数分别为(22.1±4.0)%,(20.3±4.2)%,(32.3±4.2)%和(24.7±3.8)%,明显高于溶剂对照1 d组(1.2±0.3)%(n=5,P<0.01)。AFG1处理后除d 1外,d 3,7和14肺组织抗氧化能力分别为(53.4±12.4),(42.7±10.8)和(47.2±11.0)mo.lm in-1.g-1蛋白,明显低于溶剂对照1 d组(61.9±4.3)mo.lm in-1.g-1蛋白(n=5,P<0.05)。结论AFG1对大鼠肺组织有一定的损伤作用,降低肺组织抗氧化能力,上调肺泡细胞TNFα-mRNA的表达。更多还原

【Abstract】 AIM To explore the effects of single intratracheal administration of aflatoxin G₁（AFG₁） on rat lung tissues.METHODS（Male SD rats） were intratracheally administered with AFG₁(30 μg·kg^-1),and the rats were respectively sacrificed on 1,3,7 and 14 d after AFG₁ treatment.The ultrastructural changes and the expression of TNF-α at mRNA level of lung tissues were studied with scanning electron microscopy and in situ hybridization respectively.The antioxidation capacity of lung was expressed as the decreament of H₂O₂ with biochemical method.RESULTS No differences in ultrastructural changes,TNF-α positivity as well as antioxidation capacity were observed between solvent control group and control group.Scanning microscopical observation indicated that injury changes such as,alveolar septum thickening,alveolar wall swelling changes,could be seen in lung tissues of rats 7 and 14 d after AFG₁ treatment.In situ hybridization results showed that the positive expression percentages of TNF-α in the alveolar cells in lung tissues of rats 1,3,7 and 14 d after AFG₁ treatment were（22.1±4.0）%,（20.3±4.2）%,（32.3±4.2）% and（24.7±3.8）% respectively,which were all significantly higher than that of solvent control 1 d group（1.2±0.3）%（n=5,P<0.01）.Except the rats 1 d after AFG₁ treatment,the antioxidation capacity of lung tissues in rats 3,7 and 14 d after AFG₁ treatment were（53.4±12.4）,（42.7±10.8） and（47.2±11.0）mol·min^-1·g^-1 protein,which were all significantly lower than that in solvent control 1 d group（61.9±4.3） mol·min^-1·g^-1 protein（n=5,P<0.05）.CONCLUSION Intratracheal administration of AFG₁ may cause injury and decrease the antioxidant ability in rat lung tissues,and increase the expression of TNF-α in alveolar cells.更多还原