气体信号分子硫化氢对大鼠重症急性胰腺炎肺损伤的影响  

The effect of hydrogen sulfide, a gas signaling molecule, on severe acute pancreatitis induced lung injury in rats

作　　者：王刚[1] 李乐[1] 吕嘉晨[1] 孙备[1] 武林枫[1] 周一男[1] 王大卫[1] 韩冰[1] 姜洪池[1] 

机构地区：[1]哈尔滨医科大学附属第一医院胰胆外科,150001

出　　处：《中华肝胆外科杂志》2013年第8期617-621,共5页Chinese Journal of Hepatobiliary Surgery

基　　金：基金项目：国家自然科学基金（81100314,81170481）;黑龙江省青年科学基金（QC2011C036）;中国博士后科学基金（2012M510991）;黑龙江省博士后科学基金（90857）;黑龙江省自然科学基金（D201152）;黑龙江省新世纪优秀人才培养计划（1253-NCET-017）

摘　　要：目的探讨气体信号分子硫化氢（H2S）对大鼠重症急性胰腺炎（SAP）肺损伤的影响。方法60只Wistar大鼠随机分为4组（每组15只）：假手术（sham）组、SAP组、硫氢化钠干预（NaHS）组和炔丙基甘氨酸干预（PAG）组。NaHS组和PAG组分别于造模后1h经腹腔注射NaHS和PAG。各组于造模24h后测定肺组织胱硫醚γ-裂解酶活性及mRNA表达、髓过氧化物酶、磷脂酶A2、核因子-κB活性、湿／干重比及细胞间黏附分子-1（ICAM-1）、P物质、丙二醛、肿瘤坏死因子、白细胞介素-1水平。对胰腺及肺组织进行病理学检查，检测血H2S、肿瘤坏死因子及白细胞介素-1含量。结果与SAP组相比，NaHS组各项指标均明显升高（P〈0．05），而PAG组各项指标均显著降低（P〈0．05）。结论SAP时，内源性H2S水平明显增加，对SAP并发肺损伤起到了重要的促进作用。以H2S为靶点，抑制系统和组织H2S生成对SAP继发肺损伤可起到一定的保护作用，其机制可能与抑制过度炎症反应、减轻氧化应激损伤和改善微循环障碍等有关。Objective To investigate the effect of hydrogen sulfide （H2S）, a gas signaling molecule, on severe acute pancreatitis （SAP） induced lung injury in rats. Methods A total of 60 Wistar rats were randomized into 4 groups of 15, including a sham group, SAP group, sodium bydrosulfide （NariS） group, and DL-propargylglycine （PAG） group. The rats received an intraperitoneal injection of Naris and PAG 1 hour after operation in the Naris and PAG group respectively. The remaining living animals in each group were sacrificed 24 hours after SAP models were developed to determine the pulmonary cystathionine-y-lyase （CSE） activity and mRNA expression. The myeloperoxidase （MPO）, phospholipase A2 （PLA2）, and nuclear factor κB （NF-κB）activity were evaluated. The wet dry weight ratio, as well as the levels of intercellular cell adhesion molecule 1 （ICAM-1）, substance P, maleie dialdehyde （MDA）, tumor necrosis factor α （TNF-α）, and interleukin-1β （IL 1β） were determined. The pathologic changes in the pancreas and lung were analyzed, and the serum contents of H2S, TNF-α, and IL 1β was found. Results Compared with the SAP group, every index was signifi- cantly increased in the Naris group （P〉0.05） and obviously lowered in the PAG group （P〈0.05）. Conclusion In severe acute pancreatitis, endogenous H2 S levels are obviously increased leading to sec ondary lung injury. Therefore, inhibition of systemic and tissular H2 S production may protect against SAP-induced lung injury to some extent. The mechanism of action may be related to suppressing overinflammation, abating oxidative stress, and ameliorating microcirculatory disorder.

关 键 词：胰腺炎 急性坏死性 硫化氢 肺损伤 

分 类 号：R657.51[医药卫生—外科学]