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作 者:邱兆磊[1] 王振杰[1] 郑传明[1] 周少波[2] 李磊[1]
机构地区:[1]蚌埠医学院第一附属医院急诊外科,安徽蚌埠233004 [2]蚌埠医学院第一附属医院肝胆外科,安徽蚌埠233004
出 处:《中国普通外科杂志》2012年第2期183-187,共5页China Journal of General Surgery
摘 要:目的:探讨抗肿瘤坏死因子α单克隆抗体(anti-TNF-α)对急性梗阻性黄疸大鼠心肌损伤的保护作用。方法:24只雄性SD大鼠随机均分为模型组(行胆总管结扎),治疗组(行胆总管结扎+anti-TNF-α治疗),假手术组。治疗组于胆总管结扎后第3天开始经尾静脉注射anti-TNF-α(1 mg/kg),连用5 d;模型组和假手术组以同样方法注射等体积的生理盐水。术后7 d,分别检测各组大鼠血清肌酸激酶同工酶(CK-MB)和TNF-α水平,以及大鼠心肌组织中丙二醛(MDA)和超氧化物歧化酶(SOD)含量,并观察心肌组织形态学改变。结果:除假手术组外,模型组和治疗组大鼠术后3 d开始均出现黄疸,并逐渐加重。与假手术组比较,模型组和治疗组大鼠术后7 d血清CK-MB,TNF-α水平及心肌组织中MDA含量明显升高,SOD活性明显降低(均P<0.01),但治疗组以上指标的改变不如模型组明显,差异均有统计学意义(均P<0.01)。光镜下可见假手术组心肌无明显病理改变,模型组心肌纤维稀疏、变细、坏死,心肌细胞浊肿,治疗组比模型组心肌损伤减轻。结论:TNF-α可能是急性梗阻性黄疸后大鼠心肌损伤的重要介导因子,anti-TNF-α可以通过拮抗TNF-α而减轻急性梗阻性黄疸时大鼠的心肌损伤。Objective: To investigate the protective effect of anti-TNF-α monoclonal antibody (anti-TNF-α) against the myocardial impairment induced by acute obstructive jaundice. Methods: Twenty-four male SD rats were equally randomized into the model group (undergoing common bile duct ligation), anti-TNF-α treatment group (with administration of anti-TNF-α after common bile ductligation) and sham operation group. The rats of the anti-TNF-α treatment group were injected with anti- TNF-α (1 mg/kg) through tail vein from the third postoperative day for 5 consecutive days, and those of themodel group and sham operation group were given the same volume of saline under the same administration regimen. On the seventh postoperative day, the serum level of creatine kinase (CK-MB) and TNF-α, themalondialdehyde (MDA) content and superoxide dismutase (SOD) activity in myocardial tissues of the rats were detected; the morphological changes in the myocardial tissues of the rats were also assessed. Results: Except for the sham operation group, rats in both the model group and anti-TNF-α treatment group began to present jaundice that gradually increased. The serum CK-MB and TNF-α levels and the myocardialMDA contents were significantly increased, and the myocardial SOD activities were significantly decreased on the seventh postoperative day in both the model group and anti-TNF-α treatment group compared withthe sham operation group (all P〈0.01). However, the changes of above indexes in the anti-TNF-α treatment group were less evident than those in the model group and all the differences had statistical significance (allP〈0.0 1). The myocardium from the sham operation group had no obvious pathological change under the light microscope, while the rats of the model group showed sparse atrophied cardiac muscle fibers with necrosisand cloudy swelling, and the pathological changes of myocardial impairment was relatively mild in anti-TNF-α treatment group. Conclusion: TNF-α may be a
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