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作 者:韩效帆[1] 张琼瑶[2] 张培建[1] 李鹏飞[1] 王健[1] 薛同敏[1]
机构地区:[1]扬州大学第二临床医学院普通外科研究室,江苏扬州225002 [2]重庆市第三人民医院特殊检验科,重庆400014
出 处:《中国现代普通外科进展》2014年第6期421-425,共5页Chinese Journal of Current Advances in General Surgery
基 金:江苏省扬州市社会发展科技攻关项目基金资助项目(No.YZ2010087)
摘 要:目的:探讨低氧预适应诱导热休克蛋白70(HSP70)在大鼠肝癌切除术后残肝组织调控炎症介质的作用及可能的机制。方法:制备SD大鼠种植性肝癌模型,将模型鼠随机分为假手术组(SO组)、缺血状态下肝癌切除组(IR组)和低氧预适应+缺血状态下肝癌切除组(HP组),每组20只。HP组的处理方式:术前给予10%氮氧混合气体处理90 min,Pringle法完全阻断入肝血流15 min,行肿瘤所在的肝左外叶切除。各组分别于术后1、8、12、24 h取残余肝脏标本,分别用Western blot法检测HSP70、核转录因子NF-κB p65相对表达量,ELISA法检测TNF-α、IL-1β含量,并在光镜下观察各组组织形态学改变。结果:HP组经低氧预适应后,HSP70的表达明显增加,而NF-κB p65的表达及TNF-α、IL-1β的含量均明显降低,病理损伤减轻。HSP70在SO、IR组仅有微量表达,两组间无统计学差异。结论:低氧预适应对肝癌肝切除术后缺血残肝IR损伤有保护作用,其机制可能与增加HSP70的表达,进而抑制NF-κB的活性及TNF-α、IL-1β的表达有关。Objective:TO investigate the regulation of HSP70 induced by hypoxic precondition on inflammatory mediators of the remnant livers after the hepatectomy of transplanted hepatic cancer models in SD rants and it's underlying mechanisms.Methods:Sixty SD rats of transplanted hepatic cancer models were divided into SO group,IR group and HP group,with 20 rats in each group.C group was given 10% oxygen atmosphere for 90 minutes before operation.In 15 minutes of hepatic vascular occlusion with pringle's method,the hepatectomy was performed.At 1,8,12,24 hours after operation,the relative expression of HSP70 and NF-κ B p65 and the levels of TNF-α and IL-1 β in the liver tissues were detected by Western blot and ELISA,respectively.The histopathological examination was performed.Results:HSP70 expression increased,NF-κ B p65 was decreased,the levels of TNF-α and IL-1 β and the histopathological impairment was alleviated significantly in HP group.HSP70 expression was weak in SO and IR group and had no significant differences.Conclusion:Hypoxia preconditioning have protective effect against I/R injury after the hepatectomy of transplanted hepatic cancer models in rats.The underlying mechanisms is that HP can induce HSP70 expression intensively,which can prevent the activation of NF-κ B and decrease the expression of TNF-α and IL-1β.
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