羰基硫对肢体缺血再灌注致急性肺损伤大鼠模型的作用  

Effects of carbonyl sulfide in a rat model of limb ischemia/reperfusion-induced acute lung injury

作　　者：赵彦瑞[1] 吕文睿 王东[1] 周君琳[1] 

机构地区：[1]首都医科大学附属北京朝阳医院骨科,北京市100020

出　　处：《中国组织工程研究》2016年第40期5994-6000,共7页Chinese Journal of Tissue Engineering Research

摘　　要：背景:前期研究发现,内源性气体信号分子如NO、CO、H2S及二氧化硫在急性肺损伤中发挥着重要作用,还有其他的气体参与,如羰基硫。目的:探讨外源性小剂量羰基硫对肢体缺血再灌注所致大鼠急性肺损伤的作用及其机制。方法:将64只SD大鼠随机分为8组,对照组不做处理;模型组制作肢体缺血4 h再灌注2 h损伤模型;低、中、高剂量羰基硫组分别于制作肢体缺血4 h再灌注2 h损伤模型前20 min腹腔注射0.2,0.5,1 mL羰基硫;低、中、高剂量空气组分别于制作肢体缺血4 h再灌注2 h损伤模型前20 min腹腔注射0.4,1,2 mL空气。再灌注2 h后,观察肺组织形态学及肺系数改变,应用ELISA技术检测肺组织和血清中肿瘤坏死因子α、自细胞介素1β、自细胞介素6表达,应用TUNEL技术检测细胞凋亡。结果与结论:(1)与对照组比较,模型组肺组织出现明显损伤性变化,肺系数明显增大(P<0.05),肺组织及血浆中肿瘤坏死因子α、白细胞介素1β和白细胞介素6含量增加(P<0.05),凋亡率增加;(2)与模型组比较,低、中、高剂量羰基硫可减轻肺组织损伤程度,降低肺系数及凋亡率,以低剂量效果最明显;低、中剂量羰基硫可显著降低肺组织及血浆中肿瘤坏死因子α、白细胞介素1β和白细胞介素6含量(P<0.05);(3)低、中、高剂量空气组各指标与模型组相比均无明显变化;(4)结果表明,外源性小剂量羰基硫可通过抗炎、抗氧化发挥其改善肢体缺血再灌注损伤所致急性肺损伤的作用。BACKGROUND： Previous studies have found that endogenous gaseous signaling molecules such as NO, CO, H2 S and SO2 play an important role in acute lung injury; there also have other gases participation, such as carbonyl sulfide. OBJECTIVE： To investigate the effect of carbonyl sulfide for limb ischemia-reperfusion induced acute lung injury and its mechanism in rats. METHODS： A total of 64 Sprague-Dawley rats were randomly divided into eight groups. Control group： without treatment; model group： limb ischemia for 4 hours and then reperfusion for 2 hours. Low-, moderate- and high-dose carbonyl sulfide groups were intraperitoneally injected with 0.2, 0.5, 1.0 m L carbonyl sulfide respectively at 20 minutes before ischemia for 4 hours and reperfusion for 2 hours. Low-, moderate- and high-dose air groups were intraperitoneally injected with 0.4, 1.0, 2.0 m L air respectively at 20 minutes before ischemia for 4 hours and reperfusion for 2 hours. 2 hours after reperfusion, the morphological changes of lung tissues and the change of lung coefficient were observed. The expressions of tumor necrosis factor-a, interleukin-1β and interleukin-6 both in lung tissue and serum were detected by enzyme linked immunosorbent assay. Cell apoptosis was measured by TUNEL assay. RESULTS AND CONCLUSION：（1） Compared with the control group, significant damage of lung tissue was seen, and the lung coefficient increased significantly in the model group（P〈0.05）. The expressions of tumor necrosis factor-a, interleukin-l and interleukin-6 both in lung tissue and plasma increased（P〈0.05）, and apoptotic rate increased.（2） Compared with the model group, low-, moderate- and high-doses of carbonyl sulfide could mitigate the degree of lung injury, and reduce pulmonary coefficient and apoptotic rate. The low dose showed the most obvious effect. Low- and moderate-dose carbonyl sulfide could significantly decrease expressions of tumor necrosis factor-a, interleukin-1β and interleukin-6 both in lung tissue and plasma（P�

关 键 词：实验动物 心血管及肺损伤与修复动物模型 羰基硫 缺血再灌注损伤 肿瘤坏死因子Α 白细胞介素1Β 白细胞介素6 

分 类 号：R318[医药卫生—生物医学工程]