[The therapeutic effect of carnosine combined with dexamethasone in the lung injury of seawater-drowning].

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.