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作 者:车德才[1] 李水仙[2] 武延隽[2] 赵中夫[3] 张芸[3]
机构地区:[1]山西省长治医学院生物学教研室,长治046000 [2]山西省长治医学院微生物学与免疫学教研室 [3]山西省长治医学院肝病研究所
出 处:《中国公共卫生》2007年第9期1088-1089,共2页Chinese Journal of Public Health
基 金:山西省自然科学基金(20011073)
摘 要:目的研究肿瘤坏死因子α(TNF-α)和γ-干扰素/白细胞介素4(IFN-γ/IL-4)在D-氨基半乳糖/内毒素所致大鼠急性肝衰竭中的表达。方法取30只Wistar大鼠,腹腔内注射D-氨基半乳糖/内毒素诱导大鼠急性肝衰竭模型(AHF组);另取30只腹腔内注射等量生理盐水为正常对照组(N)。2组动物于建模后3,6,12,24,48,72 h各取5只动物检测其血清丙氨酸转氨酶(ALT)并观察肝组织的病理形态学变化。酶联免疫吸附试验(ELISA)检测不同时间点动物血清中TNF-α和IFN-γ/IL-4水平的变化。结果结果显示,AHF组肝组织炎性细胞浸润和明显坏死的急性肝衰竭特征,且各时间点血清ALT值均明显高于对照组(P<0.05);AHF组与对照组比较,血清内TNF-α在3 h(P<0.01)、6 h(P<0.05)增高;IFN-γ在3 h(P<0.01)、6 h(P<0.01)增高;IL-4水平在各时间点无明显变化(P>0.05)。结论在D-氨基半乳糖/内毒素所致大鼠急性肝衰竭模型中,TNF-α和IFN-γ对急性肝衰竭早期损伤起重要作用;IL-4可能不参与此种动物模型的病理过程。Objective To research expression of sera TNF-α and IFN-γ/IL-4 in acute hepatic failure models induced by D-glactosamine and endotoxin. Methods Wistar rats with acute hepatic failure(AHF group, n = 30) were injected with saline solution. Sera Alanine Transaminase(ALT) were determined and liver pathological morphology were observed at 3, 6, 12, 24, 48, 72 h following intraperitoneal injection of D-glactosamine and endotoxin, 5 rats per time point; simultaneously, sera TNF-α and IFN-γ/IL-4 were examined by ELISA. Results Infiltration of inflammatory cells and necrosis of hepatic cells were marked in AHF group, ALT increased significantly in AHF group than in N group( P 〈 0.05) at all time points; Compared with N group, levels of sera tumor necrosis factor-α(TNF-α) in AHF group were obviously higher at 3 h( P 〈 0.01 )and 6 h(P 〈 0.05), and interferon-γ(IFN-γ) were obviously higher at 3 h( P 〈 0.01 ) and 6 h( P 〈 0.01 ) ; interleukin-4 (IL-4) weren't obviously higher at all time points( P 〉 0.05 ). Conclusion TNF-α and IFN-γ play important roles in the AHF models at early phase;However, IL-4 may not contribute to the AHF rats induced by D-glactosamine and endotoxin.
关 键 词:D-氨基半乳糖 内毒素 急笥肝衰竭 肿瘤坏死因子α(TNF-α) γ-干扰素/白细胞介素4(IFN-γ/IL-4)
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