| 王立国,郭月宁,刘喃喃,薄挽澜,庄丽维.肿瘤坏死因子α在大鼠肝肺综合征发病机制研究[J].,2021,(2):219-222 |
| 肿瘤坏死因子α在大鼠肝肺综合征发病机制研究 |
| TNF-α in the Pathogenesis of Hepatopulmonary Syndrome in Rats |
| 投稿时间：2020-07-06 修订日期：2020-07-31 |
| DOI：10.13241/j.cnki.pmb.2021.02.005 |
| 中文关键词: 肝肺综合征 内毒素 肿瘤坏死因子α 抗肿瘤坏死因子α单克隆抗体 |
| 英文关键词: Hepatopulmonary syndrome Endotoxin Tumor necrosis factor α Anti TNF-α monoclonal antibody |
| 基金项目:黑龙江省卫生计生委科研项目（2016-127） |
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| 中文摘要: |
| 摘要 目的：探讨TNF-α在大鼠肝肺综合征形成中的作用与机制。方法：采取胆总管结扎方法建立肝肺综合征模型，随机将45只大鼠分为对照组（非手术组）、模型组（胆总管结扎组）和实验组（胆总管结扎+抗TNF-α单克隆抗体组），每组15只，实验组于术后3周、4周、5周、6周分别给予腹腔注射抗TNF-α单克隆抗体；术后4周、5周、6周、7周每组每周分别处死3只大鼠，血气分析计算肺泡-动脉氧分压梯度差，测定肝纤维化指标、血浆内毒素、NO和TNF-α浓度，并进行病理组织学观察。结果：胆总管结扎术后一般4周形成肝硬化，6周形成肝肺综合征模型；实验组与模型组术后4周、5周、6周、7周肝纤维化指标HA、LN、PCⅢ、Ⅳ-C明显升高，P=0.023 (<0.05)；与模型组相比，实验组肝纤维化程度明显减轻，而对照组肝脏病理无纤维化；实验组与模型组大鼠术后4-7周内毒素、NO及TNF-α逐渐增加，呈上升趋势，与对照组相比P=0.026（<0.05），差异有统计学意义。结论：TNF-α在肝肺综合征发生发展中起到重要作用，抗TNF-α单克隆抗体可治疗肝肺综合征。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the role and mechanism of TNF-α in the formation of hepatopulmonary syndrome in rats. Methods: The model of hepatopulmonary syndrome was established by ligation of common bile duct. 45 rats were randomly divided into control group (non operation group, n=15), model group (operation group, n=15) and experimental group (operation + anti TNF-α monoclonal antibody group, n=15). 15 rats in experimental group were given intraperitoneal injection of anti TNF-α monoclonal antibody on the 3rd, 4th, 5th and 6th weeks after operation. Three rats in each group were killed on the 4th, 5th, 6th and 7th weeks after operation. The alveolar arterial oxygen pressure difference was calculated by blood gas analysis. The hepatic fibrosis indexes, level of plasma endotoxin, NO and TNF-α were detected. And histopathological observation was performed. Results: Cirrhosis was developed on the 4th week after operation of common bile duct ligation. The model of hepatopulmonary syndrome was established on the 6th week after operation. The hepatic fibrosis indexes(HA/ LN/ PCIII/ IV-C) increased significantly on the 4th, 5th, 6th and 7th weeks after operation in model and experimental group (P=0.023(<0.05)). Compared with model group, the degree of hepatic fibrosis decreased in experimental group. There was no fibrosis in control group. Compared with control group, the level of endotoxin, NO and TNF-α were increased significantly from the 4th to 7th weeks after operation in model and experimental group (P=0.026(<0.05)). Conclusion: TNF-α played an important role in the development of hepatopulmonary syndrome. Anti TNF-α monoclonal antibody can be used to treat hepatopulmonary syndrome. |
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