实验性急性肝衰竭大鼠血清中TNF-α的来源及水平变化 |
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引用本文: | 车德才,;杨苏敏,;李水仙,;武延隽,;赵中夫.实验性急性肝衰竭大鼠血清中TNF-α的来源及水平变化[J].中国实验动物学杂志,2007(7):373-376. |
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作者姓名: | 车德才 ;杨苏敏 ;李水仙 ;武延隽 ;赵中夫 |
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作者单位: | [1]长治医学院生物学教研室,长治046000; [2]长治医学院病理解剖学教研室;,长治046000; [3]长治医学院微生物学与免疫学教研室;,长治046000; [4]长治医学院肝病研究所,长治046000 |
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基金项目: | 山西省自然科学基金资助,项目编号:20011073. |
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摘 要: | 目的研究D-氨基半乳糖/内毒素所致大鼠急性肝衰竭模型中血清内TNF-α的来源及不同时间点的水平变化。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,n=30),于建模3h、6h、12h、24h、48h、72h各取5只动物检测其血清丙氨酸转氨酶(ALT)与肝组织的病理形态学变化;采用ELISA检测不同时间点动物血清中TNF-α水平的变化;通过免疫组化法检测不同时间点动物肝、肺组织内TNF-α的表达。另取30只Wistar大鼠腹腔内注射等量生理盐水为正常对照(N组,n=30)。结果AHF组各时间点血清ALT的增高与N组相比有统计学差异(P〈0.05),肝脏内炎细胞浸润、坏死明显;AHF组与N组相比血清内TNF-α的增高在3h(P〈0.01)、6h(P〈0.05)有统计学差异;AHF组肺组织与N组相比TNF-α的表达在3h、6h、12h(均为P〈0.01)有统计学差异。结论本实验成功建立了大鼠AHF模型;TNF-α在此模型的早期阶段起重要作用;肺脏可能是血清内TNF-α的主要来源之一。
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关 键 词: | D-氨基半乳糖 内毒素 急性肝衰竭 模型 肿瘤坏死因子-α(TNF-α) |
Source and Level Change of Sera TNF-α in Rats of Experimental Acute Hepatic Failure |
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Institution: | CHE De-cai, YANG Su-min, LI Shui-xian ,WU Yan-jun ,ZHAO Zhong-fu ( 1. Changzhi Medical College, Department of Biology, Changzhi 046000, China ; 2. Changzhi Medical College, Department of Pathology ; 3. Changzhi Medical College, Department of Microbiology and Immunology; 4. Changzhi Medical College ,Institute of Hepatology) |
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Abstract: | Objective To study the source and level change of sera TNF-α in D-glactosamine/endotoxin-induced acute hepatic failure models. Methods Wistar rats with acute hepatic failure (AHF group, n = 30) were induced by intrapefitoneal injection of D-glactosamine/endotoxin. To evaluate necrosis of hepatic ceils, sera Alanine Transaminase (ALT) were determined and liver pathological morphology were observed at 3 h,6 h,12 h,24 h,48 h and 72 h following intraperitoneal injection of D-glaetosamine and endotoxin, sera TNF-α were examined by ELISA; the expression of TNF-α in livers and lungs were detected by immunohistochemistry technique. Wistar rats were injected with physiological saline solution as normal controls (N group, n = 30). Results Sera ALT increased significantly in AHF group than in N group (P 〈 0.05 ) at all time points, infiltration of inflammatory ceils and necrosis of hepatic ceils were marked in AHF group; Compared with N group, levels of sera TNF-α in AHF group were obviously higher at 3 h( P 〈 0.01 ) and 6 h( P 〈 0.05) ; the expression of TNF-α in lungs in AHF group were markedly stronger than in N group at 3 h ,6 h and 12 h( P 〈 0.01 ,for these time points). Conclusion AHF rat' s models were successfully founded in our experiment; TNF-α may play important roles in the AHF models at early phase;Lungs may be the major source of sera TNF-α. |
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Keywords: | D-glactosamine Endotoxin Acute hepatic failure Model Tumor necrosis factor-α(TNF-α) |
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