Han L Y, Gao Y H, Yu G L, Shi Y, Li W P, Wang Z Q, Li Y J, Jin F G
Department of Respiratory Disease and Critical Care Medicine, the Second Affiliated Hospital, Air Force Medical University, Xi'an 710038, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2020 Sep 12;43(9):772-777. doi: 10.3760/cma.j.cn112147-20191028-00717.
To explore the therapeutic effect of carnosine and dexamethasone in lung injury caused by seawater drowning. The experiments with A549 cells were divided into 5 groups: blank control group (C), seawater injury group (S), seawater injury+dexamethasone treatment group (S+D), seawater injury+carnosine treatment group (S+C), seawater injury dexamethasone and carnosine combined therapy(S+D+C) group. The optimal therapeutic dose of drugs for the treatment of seawater drowning lung injury was tested . Based on the optimal dose, the levels of TNF-α and IL-6 in each group at different time points were detected at the cell level by ELISA. The level of apoptosis was detected by flow cytometry. The experiments with SD rats were randomly divided into 5 groups (8 each): blank control group (RC),seawater drowning injury group (RS),seawater drowning injury+dexamethasone treatment group (RSD),seawater drowning injury+carnosine treatment group (RSC),seawater drowning injury+dexamethasone+carnosine combined treatment group (RSDC). The animal model with seawater inhalation acute lung injury was made by intratracheal infusion (4 ml/kg). The pathological changes of the lungs were observed. The expression of superoxide dismutase (SOD) in each group was detected by Western blot. The results of experiments showed significant increase of apoptosis after seawater injury. The normal cell rate in group C was 98.3% while the apoptosis rate was 1.7%. The normal cell in group S was 18.8%, and the apoptosis rate was 81% (0.01). TNF-α and IL-6 levels in group S increased to 180.25 ng/L and 61.56 ng/L, respectively, which were statistically significant compared with group C (0.01). After drug protection, apoptosis was reduced in S+D group, S+C group and S+D+C group, with apoptosis rates of 65.4%, 70.9% and 42.6%, respectively. The contents of TNF-α and IL-6 also decreased in the S+D+C group (0.01). The results of experiments showed obvious lung injury and disordered lung tissue structures in the RS group at 4 h after modeling. There was hemorrhage in the pulmonary interstitium and a large number of inflammatory cells. Results of western blot showed that the expression of SOD increased in the RS group. Compared with RS group, the treatment alleviated acute lung injury and decreased the expression level of SOD in RSD, RSC and RSDC groups (0.01). Dexamethasone and carnosine reduced the influence of seawater inhalation on the lung in the rat model. The positive effect of combination of these two drugs on lung injury caused by seawater inhalation was stronger than a single drug.
探讨肌肽和地塞米松对海水淹溺致肺损伤的治疗作用。将A549细胞实验分为5组：空白对照组（C）、海水损伤组（S）、海水损伤+地塞米松治疗组（S+D）、海水损伤+肌肽治疗组（S+C）、海水损伤+地塞米松与肌肽联合治疗组（S+D+C）。测试治疗海水淹溺肺损伤的最佳药物治疗剂量。基于最佳剂量，在细胞水平通过ELISA检测不同时间点每组肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的水平。通过流式细胞术检测凋亡水平。将SD大鼠实验随机分为5组（每组8只）：空白对照组（RC）、海水淹溺损伤组（RS）、海水淹溺损伤+地塞米松治疗组（RSD）、海水淹溺损伤+肌肽治疗组（RSC）、海水淹溺损伤+地塞米松+肌肽联合治疗组（RSDC）。通过气管内注入（4 ml/kg）建立海水吸入急性肺损伤动物模型。观察肺组织的病理变化。通过蛋白质免疫印迹法检测每组超氧化物歧化酶（SOD）的表达情况。实验结果显示海水损伤后凋亡显著增加。C组正常细胞率为98.3%，凋亡率为1.7%。S组正常细胞率为18.8%，凋亡率为81%（P<0.01）。S组TNF-α和IL-6水平分别升高至180.25 ng/L和61.56 ng/L，与C组相比差异有统计学意义（P<0.01）。药物保护后，S+D组、S+C组和S+D+C组凋亡减少，凋亡率分别为65.4%、70.9%和42.6%。S+D+C组TNF-α和IL-6含量也降低（P<0.01）。实验结果显示建模后4小时RS组肺损伤明显，肺组织结构紊乱。肺间质有出血，并有大量炎性细胞。蛋白质免疫印迹结果显示RS组SOD表达增加。与RS组相比，治疗减轻了急性肺损伤，RSD、RSC和RSDC组SOD表达水平降低（P<0.01）。地塞米松和肌肽减轻了大鼠模型中海水吸入对肺的影响。这两种药物联合对海水吸入所致肺损伤的积极作用强于单一药物。
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