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

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，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（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。

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

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.