ABSTRACT
This paper aimed to study the protective effect of ginsenoside Rg_1 on endotoxin(LPS)-induced apoptosis of lung epithelial cells and its mechanism of action. Mouse lung epithelial cells(MLE-12) were first treated with LPS. The autophagy changes and apoptosis and the relationship with concentration and time of LPS were observed. Then,the level of autophagy in MLE-12 was regulated at a specific concentration and action time of LPS,and the changes of apoptosis were observed. Secondly,ginsenoside Rg_1 and autophagy inhibitor 3-MA were added respectively at the same concentration and action time of LPS. The lung epithelial cells were grouped to observe the effect of ginsenoside Rg_1 on LPS-induced apoptosis of lung epithelial cells and its mechanism. In the animal experiment,the mice were grouped and tested by apoptosis protein,lung injury score and HE staining section to verify whether ginsenoside Rg_1 has a protective effect on LPS-induced lung injury. The results showed that apoptosis and autophagy increased as the rise of concentration after treatment with LPS for 12 h. The apoptosis increased gradually,and the autophagy increased first and then decreased over time at the LPS concentration of 25 g·L-1. The apoptosis of LPS group was higher than that of control group,and LPS+3-MA group increased further,while apoptosis decreased significantly in LPS+RAM(rapamycin,autophagy promoter) group. The autophagy increased in LPS group,decreased in LPS+3-MA group and increased in LPS+RAM group. The apoptosis of LPS group was higher than that of control group,and the apoptosis of LPS+Rg_1 group decreased. The apoptosis of LPS+Rg_1+3-MA group increased again. The autophagy of LPS group further increased after administration of ginsenoside Rg_1,but decreased after administration of 3-MA. In the in vivo experiments in mice,the apoptosis of LPS group increased significantly compared with the control group,while LPS + ginsenoside Rg_1 group decreased. Lung injury score and HE staining also conformed to the above trend. LPS can induce the apoptosis of lung epithelial cells in a time-dependent and concentration-dependent manner. The autophagy of lung epithelial cells increases with the rise of LPS concentration. At the specific concentration of LPS,autophagy increases first and then decreases after 12-16 hours. Proper increase of autophagy in lung epithelial cells within a certain period of time can reduce the apoptosis induced by LPS,while inhibition of autophagy can increase apoptosis. Ginsenoside Rg_1 has a protective effect on lung cancer epithelial cell apoptosis induced by autophagy.
Subject(s)
Animals , Mice , Apoptosis , Autophagy , Cells, Cultured , Epithelial Cells , Ginsenosides , Pharmacology , Lipopolysaccharides , Lung , Cell BiologyABSTRACT
Objective The level of lactic acid in blood can reflect the degree of ischemia and hypoxia of brain tissue and cerebral perfusion pressure. The aim of this paper is to explore the value of blood lactate and lactate clearance in evaluating the survival rate and neurological outcome of patients with craniocerebral trauma. Methods The clinical data of 497 craniocerebral trauma patients admitted to our hospital from September 2017 to July 2018 were collected and retrospectively analyzed. Patients were divided into groups with different 6 h lactate clearance rates and admission lactate levels, and the differences in mortality and outcome of neurological function in each group were compared. Results The serum admission lactate levels、serum lactate levels at 6 hours, 28-day mortality and 28-day poor nerve function prognosis rate of patients with different 6h lactate clearance rates were statistically significant differences(P < 0. 05). The efficacy of 6h lactic acid to predict the mortality rate of patients was better than that of admission lactic acid and 6h lactate clearance rate (Z=3.71、Z=3.95,P<0.05). However, in predicting the neurological function of patients, the lactate clearance rate is not better than blood lactate level at any time(Z=1.30，Z=0.81，P>0.05). Conclusion 6h lactic acid has the best ability to judge the mortality of patients while lactic acid clearance rate is not better than the blood lactate level at any time in predicting the neurological function of patients.
ABSTRACT
Objective Prone position ventilation is one of the most important Methods for the treatment of acute lung injury/acute respiratory distress syndrome (ARDS). Currently, there are fewer researches on prone position ventilation for ARDS caused by acute paraquat poisoning. This article aims to evaluate the value of prone position ventilation in the treatment of moderate and severe ARDS caused by acute paraquat poisoning.Methods Retrospective analysis the clinical data of 43 patients with acute paraquat poisoning complicated with moderate-to-severe ARDS from January 2016 to December 2017 in the Department of Emergency Medicine, Eastern Theater of the Eastern Theater. The patients were divided into two groups according to whether they were in prone position ventilation: experimental group (prone position ventilation, n=13)and control group(no prone position ventilation, n=30). The gender, age, APACHEII score and plasma paraquat concentration of the two groups were statistically analyzed. The oxygenation index, respiratory rate, carbon dioxide partial pressure and mean arterial pressure were compared between the two groups during the first five days after hospitalization. At the same time, the hospital mortality, hospitalization time, mechanical ventilation time were also compared.Results Compared with control group, the oxygenation index (176±13) and carbon dioxide partial pressure \[(33.6±4.3) mmHg\] in the experimental group were significantly increased from the 2nd day to 5th day after hospitalization(P0.05).Conclusion Prone position ventilation is safe for patients with moderate to severe ARDS caused by acute paraquat poisoning, which improves oxygenation in these patients but fails to improve prognosis. It provides a theoretical basis for prone position ventilation in the treatment of acute paraquat poisoning complicated with ARDS.