Protective Mechanism Of Tripterine On Acute Lung Injury Induced By Inhaling Hydrochloric Acid In Mice

Objective: Acute lung injury in perioperation is a common clinical complication,one leading cause of which is aspiration of acid into airway.The mainstay of current treatment in such patients includes machanical ventilation,high—inspired concentrations of oxygen and myeloperoxidase therapy etc.However,the treatment effect is unsatisfactory.This study attempts to provide a theoretical basis for the clinical treatment by observing the protective effect of the pre administration of tripterine on lung injury induced by inhalation of hydrochloric acid,and then investigate the protective mechanism of tripterine on acute lung injury induced by inhaling hydrochloric acid in mice.Methods: 24 health mice were divided into 4 groups at random(n = 6): Group A,the normal control group;Group B,tripterine by intraperitoneal injection;Group C,hydrochloric acid inhalation group;Group D: hydrochloric acid inhalation + tripterine by intraperitoneal injection.Four groups of mice were treated with intraperitoneal injection for 3 days in advance,group A and group C received 3ml/kg saline by intraperitoneal injection once a day,group B and group D received 3mg/kg(about 3ml/kg)tripterine by intraperitoneal injection once a day.At the beginning of the experiment,the four groups of mice fasted 12 h but can not refrain the water.They were anesthetized by intraperitoneal injection of pentobarbital sodium(50mg/kg),and then intubate the outer tube of trocar 24 into trachea.Group C and group D were injected with hydrochloric acid(PH=1.5,2ml/kg),then injected a small amount of air into the lungs to make the acute lung injury model.group A and group B were injected with the same amount of saline and air.And then the tube was removed from the mice mouth and allowed the mice to freely access water and food.The model of acute lung injury was made by intratracheal instillation of hydrochloric acid in mice.The mice were sacrificed at 6h after instillation of hydrochloric acid and the lung tissue were taken out.To observe the change of pathology in mice lung tissue 6h after the hydrochloric acid was inhaled and at the same time,to detect the change of SOD activity and MDA content,TNF-? content IL-6content,as well as the change of the MIF,MPO level in lung tissue.Results(1)The pathological results from the lung tissue showed that: compared with the group C,the lung tissue of group D was clear,inflammatory cell infiltration and hemorrhage were significantly reduced.(2)Compared with the group A,the MDA content of group C?group D were increased(P<0.01),the SOD activity of group C?group D were decreased(P<0.01);and the MDA content of group C was increased than the group D(P<0.01),the SOD activity of group C was decreased than the group D(P<0.01).(3)TNF-? content and IL-6 content were lower in group A and group B,group C was the highest,and group D was in the middle.Compared with the group A,the TNF-? contentand IL-6 content of group C and group D were higher;the TNF-? content and IL-6content of group C were increased than that of group D(P<0.01).(4)MIF and MPO content were lower in group A and group B,group C was the highest,and group D was in the middle.Compared with the group A,the MIFcontent and the MPO content of group C and group D were higher(P<0.01);the MIF content and MPO content of group C were increased than that of group D(P<0.01).Conclusion 1.Hydrochloric—acid aspiration may induce an acute and diffuse lung injury,manifesting with tachypnea,,lower Pa02 and severe pathologicalchanges in lung tissues.2.Locally the imbalanced oxidative / antioxidative reaction and increased inflammatory cytokines(such as TNF-??IL-6)formation play an important roles in the pathogenesis of hydrochloric acid—induced lung injury.3.Tripteryine has a protective effect on acute respiratory distress syndrome induced by inhaling hydrochloric acid in mice,the mechanism may involved inhibiting macrophage migration inhibitory factor(MIF)expression,reducing neutrophil infiltration,reducing oxidative damage and reduced inflammation injury.