CAJ | 학술논문

目的:探讨硫化氢(H_2S)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,5 mg/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6 h测定大鼠动脉血氧分压(PaO_2);检测肺组织中H_2S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PaO_2显著下降并出现肺组织结构损伤,而肺组织中H_2S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PaO_2显著升高,肺组织结构损伤明显减轻,肺组织中H_2S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H_2S的生成减轻脂多糖性肺损伤.
목적:탐토류화경(H_2S)재팔태담낭수축소(CCK-8)개선지다당성폐손상중적작용.방법:용정맥주사지다당(LPS,5 mg/kg)법제비대서폐손상모형,장웅성Wistar대서수궤분위정상대조조、LPS조、LPS+CCK-8조급CCK-8조.급약후6 h측정대서동맥혈양분압(PaO_2);검측폐조직중H_2S함량화광류미-γ-렬해매(CSE)활성;RT-PCR검측폐조직CSE mRNA적표체;광경관찰폐조직적형태학변화.결과:여정상대조조상비,LPS조대서PaO_2현저하강병출현폐조직결구손상,이폐조직중H_2S함량、CSE활성화mRNA표체현저증고(균P<0.05);여LPS조상비,LPS+CCK-8조대서PaO_2현저승고,폐조직결구손상명현감경,폐조직중H_2S함량화CSE활성급mRNA표체현저하강(균P<0.05);CCK-8조대서상술각지표여정상대조조상비무명현차이.결론:CCK-8가통과억제내원성H_2S적생성감경지다당성폐손상.
AIM: To investigate the role of hydrogen sulfide (H_2S) 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 (PaO_2), H_2S 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 PaO_2 level, increased index of quantitative assessment (IQA) score, while H_2S 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 PaO_2 level and alleviated the degree of lung injury (measured by IQA score). In addition, CCK-8 decreased H_2S 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 H_2S.