中国组织工程研究

中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (31): 5823-5827.doi: 10.3969/j.issn.2095-4344.2012.31.026

• 器官移植基础实验 basic experiments of organ transplantation • 上一篇    下一篇

硫化氢增加肝脏缺血再灌注损伤模型大鼠胰岛素样生长因子Ⅰ、 核转录因子κB、肿瘤坏死因子α的表达

王海久，任 利，邓 勇，王 聪，李衍飞，阳丹才让，樊海宁   

  1. 青海大学附属医院肝胆胰外科，青海省西宁市 810001
  • 收稿日期:2012-04-13 修回日期:2012-05-19 出版日期:2012-07-29 发布日期:2012-07-29
  • 通讯作者: 樊海宁，硕士，教授，青海大学附属医院肝胆胰外科，青海省西宁市 810001 fanhaining@medmail.com.cn
  • 作者简介:王海久★，男，1970年生，青海省乐都县人，汉族，硕士，副教授，主要从事肝纤维化方面的研究。 wanghaijiuqh@163.com

Hydrogen sulfide increases the expression of insulin-like growth factor Ⅰ, nuclear factor kappa B and tumor necrosis factor alpha in a rat hepatic ischemia-reperfusion injury model

Wang Hai-jiu, Ren Li, Deng Yong, Wang Cong, Li Yan-fei, Yangdan Cai-rang, Fan Hai-ning   

  1. Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qinghai University, Xining 810001, Qinghai Province, China
  • Received:2012-04-13 Revised:2012-05-19 Online:2012-07-29 Published:2012-07-29
  • Contact: Fan Hai-ning, Master, Professor, Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qinghai University, Xining 810001, Qinghai Province, China fanhaining@medmail.com.cn
  • About author:Wang Hai-jiu★, Master, Associate professor, Department of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Qinghai University, Xining 810001, Qinghai Province, China wanghaijiuqh@163.com

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摘要：

背景：硫化氢气体是一种新型气体信号分子，在生理浓度下具有抑制Ca2+内流、开放KATP通道功能，氧化还原等明确特定的作用。
目的：观察硫化氢对大鼠肝脏缺血再灌注损伤胰岛素样生长因子Ⅰ、核转录因子κB及肿瘤坏死因子α表达水平的影响
方法：70只SD大鼠随机等分为假手术组、缺血20 min组，缺血20 min+灌注2，4 h组、硫氢化钠+缺血20 min组、硫氢化钠+缺血20 min再灌注2，4 h组。除假手术组外，其余各组大鼠通过Pringle法建立大鼠全肝缺血再灌注模型，在术前5 d中每天及术中向硫氢化钠+缺血20 min组、硫氢化钠+缺血20 min再灌注2，4 h组，大鼠腹腔注射56 μmol/kg 硫氢化钠。
结果与结论：肝脏缺血大鼠肝组织中胰岛素样生长因子Ⅰ 、核转录因子κB和肿瘤坏死因子α表达明显下降(P < 0.05)，与缺血组比较，大鼠再灌注和腹腔注射硫化氢均能增加大鼠肝组织中胰岛素样生长因子Ⅰ 、硫化氢、核转录因子κB和肿瘤坏死因子α的表达(P < 0.05)。提示全肝缺血再灌注后可造成肝脏损伤，硫化氢增加肝脏缺血再灌注损伤模型大鼠胰岛素样生长因子Ⅰ、核转录因子κB、肿瘤坏死因子α的表达，肝脏损伤具有保护作用。

关键词: 硫化氢, 肝脏缺血再灌注损伤, 胰岛素样生长因子Ⅰ, 核转录因子κB, 肿瘤坏死因子α

Abstract:

BACKGROUND: Hydrogen sulfide is a novel gaseous signal molecule, which can inhibit Ca2+ influx, open KATP channel and balance oxidation-reduction and exert other specific functions at physiological concentrations.
OBJECTIVE: To observe the effect of hydrogen sulfide on the expression of insulin-like growth factor Ⅰ, nuclear factor κB and tumor necrosis factor α in the rat hepatic ischemia-reperfusion injury model.
METHODS: Seventy SD rats were randomly divided into seven groups: sham operation, 20-minute ischemia group, 20-minute ischemia+2 and 4 hours reperfusion group, sodium hydrosulfide+20-minute ischemia group, and sodium hydrosulfide+20-minute ischemia+2 and 4 hours reperfusion group. Hepatic ischemia-reperfusion model were established by Pringle method for each group except the sham operation group. Sodium hydrosulfide+20-minute ischemia group and sodium hydrosulfide+20-minute ischemia+2 and 4 hours reperfusion group were intraperitoneally injected with 56 μmol/kg sodium hydrosulfide each day for the 5 days before surgery.
RESULTS AND CONCLUSION: The expression of insulin-like growth factor Ⅰ, nuclear factor κB and tumor necrosis factor α were significantly decreased in the ischemic rat liver tissue (P < 0.05); in comparison with the ischemia groups, both reperfusion and intraperitoneal injection of sodium hydrosulfide could significantly increase the expression of insulin-like growth factorⅠ, nuclear factor κB and tumor necrosis factor α (P < 0.05). It suggests that reperfusion after whole-liver ischemia can cause liver damage, and sodium hydrosulfide can protect the liver by increasing the expression of insulin-like growth factor Ⅰ, nuclear factor κB and tumor necrosis factor α in rat hepatic ischemia-reperfusion injury model.

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