内源性硫化氢对硫酸铍致大鼠肺组织急性损伤影响  

Effects of endogenous hydrogen sulfide on acute lung injury induced by beryllium sulfate in rats

作　　者：廖永红[1] 黄炼[1] 王淑娟[1] 胡立丹 张朝晖[1] 

机构地区：[1]南华大学公共卫生学院环境医学与放射卫生研究所,湖南衡阳421001

出　　处：《中国职业医学》2013年第5期403-406,410,共5页China Occupational Medicine

基　　金：湖南省科技厅资助项目(2011TT2013);南华大学博士启动基金(2013XQ);衡阳市科技局资助课题(2011ks11)

摘　　要：目的探讨内源性硫化氢(H2S)对硫酸铍(BeSO4)致大鼠肺组织急性损伤的作用及可能机制。方法 48只雄性无特定病原体级SD大鼠随机分为对照组、BeSO4组、[BeSO4+硫氢化钠(NaHS)]组和[BeSO4+DL-炔丙基甘氨酸(PPG)]组,每组12只。对照组一次性给予气管内滴注0.001 ml/g体质量灭菌生理氯化钠溶液,30 min后腹腔注射灭菌生理氯化钠溶液0.010 ml/g体质量;其余3组均气管内滴注质量浓度为12 g/L的BeSO4灭菌生理生理氯化钠溶液,30 min后分别腹腔注射灭菌生理氯化钠溶液、浓度为14μmol/L NaHS灭菌生理氯化钠溶液和质量浓度为37.5 g/L PPG灭菌生理氯化钠溶液。7周后颈动脉放血处死大鼠,检测活性氧(ROS)和血浆及肺组织中H2S水平;收集支气管肺泡灌洗液(BALF)进行炎性细胞计数;观察肺组织病理形态及超微结构变化。结果与对照组比较,BeSO4组、(BeSO4+NaHS)组和(BeSO4+PPG)组肺脏系数、ROS水平及BALF中炎性细胞数均升高(P<0.05);血浆及肺组织中H2S水平均降低(P<0.05);BeSO4组、(BeSO4+NaHS)组和(BeSO4+PPG)组肺组织均可见大量炎性细胞浸润,纤维组织及巨噬细胞增生,甚至坏死;肺组织超微结构损伤明显。结论内源性H2S对BeSO4致大鼠肺组织损伤具有保护作用,其机制可能与内源性H2S调节炎症反应,减少ROS的生成有关。Objective To investigate the effects and mechanisms of endogenous hydrogen sulfide on acute lung injury in- duced by beryllium sulfate （ BeSO4 ） in rats. Methods Forty-eight SPF male SD rats were randomly divided into 4 groups, including a control group, a BeSO4 group, a [ BeSO4 ＋ sodium hydrosulfide （NariS） ] group and a [ BeSO4 ＋ DL-proparg- ylglycine （PPG） ] group （n = 12）. The control group was treated with non-exposed intratracheal instillation （0.001 ml/g · BW） of sterile saline, 30 minutes later, intraperitoneal injection （0. 010 ml/g · BW） of sterile saline, others were administrated by intratracheal instillation of 12 g/L BeS04, 30 minutes later, sterile saline, 14 μmol/L NariS and 37.5 g/L PPG were injected ip respectively. After 7 weeks, rats were sacrificed, the levels of H2S in plasma and lung tissue and reactive oxygen species （ROS） level were detected, the bronchoalveolar lavage fluid （BALF） was collected to inflammatory cell count; the pathomorphological and ultrastructure changes of lung tissue were observed. Results Compared with those of the control group, lung coefficient, level of ROS and the number of inflammatory ceils in BALF significantly increased （P 〈 0.05） ; the levels of H2 S in the plasma and lung tissue decreased （P 〈 0. 05 ）. Compared with those of the control group, inflammatory cell infiltration, proliferation of fibrous tissue and macrophages, or necrosis were seen and ultrastructure damage was obvious in lung tissue. Conclusion Endogenous H2S exerts protective effect on acute lung injury of BeSO4-induced rats, the mechanism may be related to the regulation of inflammation and reduce of ROS generation.

关 键 词：硫酸铍 硫化氢 大鼠 肺组织损伤 支气管肺泡灌洗液 

分 类 号：R114[医药卫生—卫生毒理学]