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丙酮酸乙酯对烫伤延迟复苏大鼠肾组织高迁移率族蛋白B1表达和急性肾损伤的影响

ISSN号：0529-5815
期刊名称：《中华外科杂志》
时间：0
分类：R631.02[医药卫生—临床医学;医药卫生—外科学]
作者机构：[1]第四军医大学西京医院肝胆外科,西安710032, [2]解放军总医院第一附属医院烧伤研究所, [3]武警北京总队医院
相关基金：国家重点基础研究发展规划项目（2005CB522602）;国家杰出青年科学基金资助项目（30125020）;国家自然科学基金资助项目（30672178）

作者：王强[1], 姚咏明[2], 王彦博[3], 王文江[2,3], 咸力明[2], 窦科峰[2], 盛志勇[2]

关键词：烧伤, 丙酮酸乙酯, 高迁移率族蛋白B1, 急性肾损伤, Burns, Ethyl pyruvate, High mobility group box-1 protein, Acute kidney injury

中文摘要：

目的观察丙酮酸乙酯（EP）对烫伤延迟复苏大鼠肾组织高迁移率族蛋白B1（HMGB1）表达及急性肾损伤的影响。方法采用30％体表面积Ⅲ度烫伤延迟复苏大鼠模型，78只大鼠随机分为假伤组（n=18）、烫伤组（n=30）和EP治疗组（n=30）；采用逆转录聚合酶链反应检测各组大鼠肾组织HMGB1 mRNA表达，蛋白印迹法及免疫组化法检测。肾组织HMGB1蛋白表达；同时测定血尿素氮（BUN）含量并观察。肾组织病理变化。结果与假伤组比较，严重烫伤后。肾组织HMGBl基因／蛋白表达于伤后8～72h显著增强（P〈0．05），BUN含量在伤后8h及24h显著升高（P〈0．05）。与烫伤组比较，EP治疗组肾组织8、24、72h时HMGBl表达均显著下调，BUN含量在8、24h时亦明显下降（P〈0．05）；光镜下观察烫伤组肾组织炎性细胞浸润，肾小管结构破坏出现浊肿、变性，而EP处理后。肾脏病理改变不同程度地减轻。结论HMGB1作为晚期炎性因子参与了烫伤后。肾组织炎症反应的病理过程，应用EP治疗可有效下凋。肾组织HMGB1表达，并显著减轻烫伤延迟复苏所致的急性肾损伤。

英文摘要：

Objective To investigate the effect of ethyl pyruvate （EP） on high mobility group box- 1 protein（ HMGB1 ） expression in renal tissue and acute kidney injury in rats with delayed resuscitation after thermal injury. Methods Seventy-eight Wistar rats subjected to 30% total body surface area full-thickness thermal injury followed with delayed resuscitation were divided into 3 groups： sham group（ n = 18 ） , injury group （n = 30） and EP group（ n = 30 ）. Renal tissue and blood samples were harvested to determine HMGB1 mRNA as well as its protein expression and renal function parameter at the 8, 24, 72 h post the ＂injury＂. HMGB1 mRNA was semi-quantitatively measured by reverse transcription polymerase chain reaction taking GAPDH as an internal standard, and HMGB1 protein expression was determined by Western blot and immunohistochemistry. Blood urea nitrogen （BUN） levels were measured with automatic biochemistry analyzer. The pathological changes of renal tissues were examined using HE staining. Results Compared with sham controls, both mRNA and protein expressions of HMGB1 in injury group were significantly enhanced in kidneys at 8-72 h after thermal injury （P 〈 0.05 ） , meanwhile serum BUN levels were markedly increased （ P 〈 0. 05 ）. Compared with injury group, the renal HMGB1 mRNA and protein expressions were markedly down-regulated in EP group at 8 h, 24 h and 72 h post injury （ P 〈 0. 05 ） , respectively, and meanwhile serum BUN levels were reduced significantly（ P 〈 0.05 ）. Inflammatory cell infiltration was found in renal tissues following injury, and kidney injury was markedly alleviated after treatment with EP. Conclusions It indicated that HMGB1 appears to be involved in the pathogenesis of post-burn acute kidney injury. Treatment with EP reduces renal HMGB1 expression, and protects against acute kidney injury secondary to delayed resuscitation after major burns.

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