CAJ | 학술논문

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24 h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.
목적 탐토기체신호분자류화경(H2S)대대서중증급성이선염(SAP)폐손상적영향.방법 60지Wistar대서수궤분위4조(매조15지):가수술(sham)조、SAP조、류경화납간예(NaHS)조화결병기감안산간예(PAG)조.NaHS조화PAG조분별우조모후1h경복강주사NaHS화PAG.각조우조모24 h후측정폐조직광류미γ-렬해매활성급mRNA표체、수과양화물매、린지매A2、핵인자κB활성、습/간중비급세포간점부분자-1(ICAM-1)、P물질、병이철、종류배사인자、백세포개소-1수평.대이선급폐조직진행병이학검사,검측혈H2S、종류배사인자급백세포개소-1함량.결과 여SAP조상비,NaHS조각항지표균명현승고(P＜0.05),이PAG조각항지표균현저강저(P＜0.05).결론 SAP시,내원성H2S수평명현증가,대SAP병발폐손상기도료중요적촉진작용.이H2S위파점,억제계통화조직H2S생성대SAP계발폐손상가기도일정적보호작용,기궤제가능여억제과도염증반응、감경양화응격손상화개선미순배장애등유관.
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 hydrosulfide (NaHS) group,and DL-propargylglycine (PAG) group.The rats received an intraperitoneal injection of NaHS and PAG 1 hour after operation in the NaHS 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-γ-1yase (CSE) activity and mRNA expression.The myeloperoxidase (MPO),phospholipase A2 (PLA2),and nuclear factor-κB (NF-κB)activity were evaluated.The wetdry weight ratio,as well as the levels of intercellular cell adhesion molecule-1 (ICAM-1),substance P,maleic 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 significantly increased in the NaHS group (P＜0.05) and obviously lowered in the PAG group (P＜0.05).Conclusion In severe acute pancreatitis,endogenous H2S levels are obviously increased leading to secondary 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.