CCK-8对脂多糖性肺损伤大鼠肺组织中硫化氢生成的抑制作用  

Inhibitory effect of cholecystokinin-octapeptide on production of hydrogen sulfide in lung of LPS-induced lung injury rats

作　　者：黄新莉[1] 周晓红[1] 田凤军[1] 羡晓辉[1] 凌亦凌[1] 

机构地区：[1]河北医科大学病理生理教研室,河北石家庄050017

出　　处：《中国病理生理杂志》2010年第2期309-313,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30800440);河北省自然科学基金资助项目(No.C2007000830;No.C2008001040);北京市自然科学基金资助项目(No.7092035)

摘　　要：目的:探讨硫化氢(H2S)在八肽胆囊收缩素(CCK-8)改善脂多糖性肺损伤中的作用。方法:用静脉注射脂多糖(LPS,5mg/kg)法制备大鼠肺损伤模型,将雄性Wistar大鼠随机分为正常对照组、LPS组、LPS+CCK-8组及CCK-8组。给药后6h测定大鼠动脉血氧分压(PaO2);检测肺组织中H2S含量和胱硫醚-γ-裂解酶(CSE)活性;RT-PCR检测肺组织CSE mRNA的表达;光镜观察肺组织的形态学变化。结果:与正常对照组相比,LPS组大鼠PaO2显著下降并出现肺组织结构损伤,而肺组织中H2S含量、CSE活性和mRNA表达显著增高(均P<0.05);与LPS组相比,LPS+CCK-8组大鼠PaO2显著升高,肺组织结构损伤明显减轻,肺组织中H2S含量和CSE活性及mRNA表达显著下降(均P<0.05);CCK-8组大鼠上述各指标与正常对照组相比无明显差异。结论:CCK-8可通过抑制内源性H2S的生成减轻脂多糖性肺损伤。AIM： To investigate the role of hydrogen sulfide （H2S） in the cholecystokinin octapeptide （CCK -8） attenuating lipopolysaccharide （LPS） -induced lung injury. METHODS： A rat model of lung injury induced by intravenous injection of LPS was developed. Male Wistar rats were divided into normal control group, LPS group, LPS ＋ CCK -8 group and CCK- 8 group. Six hours after LPS injection, partial pressure of oxygen in the arterial blood （PaO2）, H2S content and cystathionine -γ - lyase （ CSE ） activity in lung tissue were detected. The mRNA expression of CSE in lung tissue was determined by RT - PCR; the structure of lung tissues was observed under optical microscope. RESULTS： Compared to normal control rats, the LPS - treated rats had significantly decreased PaO2 level, increased index of quantitative assessment （IQA） score, while H2 S content, CSE activity and the mRNA expression of CSE in lung tissue were significantly increased （ all P 〈 0. 05 ）. Administration of CCK - 8 into LPS - treated rats increased the PaO2 level and alleviated the degree of lung injury （measured by IQA score）. In addition, CCK -8 decreased H2S content, CSE activity, and the mRNA expression of CSE （all P 〈0. 05）. No significant difference of the above- mentioned parameters between CCK- 8 group and normal control group was observed. CONCLUSION ： CCK - 8 reduces LPS induced lung injury through inhibiting the generation of endogenous H2 S.

关 键 词：胆囊收缩素 硫化氢 脂多糖类 肺损伤 大鼠 

分 类 号：R363.2[医药卫生—病理学]