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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 effect and possible mechanism of endogenous hydrogen sulfide (H2S) on acute lung injury induced by beSO4 in rats. Methods 48 male SD rats without specific pathogen were randomly divided into control group, BeSO4 group, [BeSO4 + sodium hydrosulfide (NaHS)] group and [BeSO4 + DL-propargylglycine (PPG) . The control group was given intraperitoneal instillation of 0.001 ml / g body weight sterilized physiological sodium chloride solution once a day, and injected with sterilized physiological sodium chloride solution 0.010 ml / g intraperitoneally 30 minutes after the endotracheal intubation. The other three groups were given intratracheal instillation BeSO4 sterilized physiological and physiological sodium chloride solution with mass concentration of 12 g / L was injected intraperitoneally into sterile physiological sodium chloride solution at a concentration of 14μmol / L NaHS sterile physiological sodium chloride solution and the mass concentration was 37.5 g / L PPG sterile physiological sodium chloride solution. After 7 weeks, the rats were sacrificed by carotid artery exsanguination. The levels of reactive oxygen species (ROS) and H2S in plasma and lung tissue were measured. The bronchoalveolar lavage fluid (BALF) was collected for inflammatory cell counting. The pathological changes and ultrastructural changes . Results Compared with the control group, the lung coefficient, ROS level and the number of inflammatory cells in BALF in BeSO4 group, BeSO4 + NaHS group and BeSO4 + PPG group were significantly increased (P <0.05). The levels of H2S in plasma and lung tissue (P <0.05). In the BeSO4 group, the BeSO4 + NaHS group and the BeSO4 + PPG group, a large number of inflammatory cell infiltration, fibrous tissue and macrophage proliferation and even necrosis were observed. The ultrastructure of lung tissue Damage is obvious. Conclusions Endogenous H2S can protect BeSO4-induced lung injury in rats. The mechanism may be related to the regulation of inflammatory reaction by endogenous H2S and the reduction of ROS production.