Differently Hypoxic Exposure Effects On The Expression Levels Of COX-I Gene In Myocardial Tissue With The Rats Simulated At An Altitude Of 5000 M

Objective: Cold and hypoxia composed of the complex environment, which posed the severer health damage to people who have the long-term living in the plateau in Qinghai-Tibetan Plateau. Sea-level people into the plateau low oxygen environment will happen in the body after a series of changes to adapt to the specific environment, will happen some degree different altitude sickness and suffering from altitude sickness, so that decreased the labor ability, which is low oxygen environment acclimatization of poor performance on the plateau. Chronic Mountain sickness is unique to the Qinghai-Tibet plateau, its pathological physiological characteristics for severe hypoxemia, red blood cell excessive proliferation and persistent pulmonary hypertension, if not treated in time, will lead to right heart function failure. Actively seek to promote plateau acclimatization and the prevention and control measure of altitude sickness is the focus of the current plateau medical research and cutting edge. Research data show that the plateau residents imbalance in the body there is a certain degree of energy metabolism, are some of the plateau disease one of the important reasons of the occurrence and development.Cytochrome C oxidase cytochrome C oxidase(COX), play a key role in the process of energy metabolism of cells, catalyzed electrons from the reduction of cytochrome C transferred to the mitochondria to form oxygen. This topic with the same altitude at different time of hypoxia in rats as the research object, the determination of the experimental group and control group rats myocardial tissue of mitochondrial cytochrome oxidase activity and sub I. the differences of protein expression, in order to make clear the same altitude at different time rat myocardial tissue hypoxia of mitochondrial cytochrome oxidase activity and sub I. the differences of protein expression and the possible mechanism of the influence of low oxygen and hypoxic acclimatization and plateau adaptation mechanism and the relationship between radical plateau people how to provide certain theoretical basis for prevention of altitude sickness.Method: Male Wistar rats were randomly divided into plains in the control group, hypoxia group 3d, 7d, 15 d and 30 d, 15 in each group. Hypoxic rats in low pressure chamber simulation at an altitude of 5000 m plateau. to the point in time after the cabin materials, the control group rats in extravehicular materials immediately. Take out the part after myocardial tissue by real-time fluorescent quantitative PCR methods to analyze mitochondria(COX- I) gene expression, another part of the line in optical electronic microscope after HE staining myocardial tissue morphology. ELISA methods were conducted to measure the serum levels of HIF, ROS, SOD and CAT levels.Result: 1、3, 7 and when hypoxia 15 d, COX activity continued to decrease in myocardial tissue, and the control group, the difference was statistically significant(P <0.05); hypoxia 30 d, COX activity increased hypoxia 15 d group difference was statistically significant(P <0.05), but still lower than that of control group(P <0.05). 2、during hypoxia, myocardial tissue mitochondrial protein COX I did not change significantly, each group with that of control group was not significant compared with no significant difference between the two groups. 3、hypoxia 30 d, the increased serum levels of HIF-1 expression, and the control group, hypoxia 3d, 7d hypoxia group, the difference was statistically significant(P <0.05). 4 、expression in rat serum ROS levels were significantly lower during hypoxia 30 d, there was significant(P <0.05) difference compared with the control group. 5、in the long term a low oxygen environment, compared with the control group, hypoxia group serum SOD and CAT levels were not significantly increased, there was no significant difference between the two groups. 6、HE staining showed that the longer the hypoxic myocardial cells gradually decrease the number of mitochondria, irregular, disorganized, or even destroy the cell structure.Conclusion: 1, acute myocardial tissue hypoxia decreased the expression of COX activity of mitochondria, mitochondrial chronic hypoxia myocardial tissue expression of COX activity has been restored. 2, acute hypoxia mitochondrial function is suppressed, the longer hypoxia mitochondrial dysfunction more serious. 3, the expression level of tissue hypoxia ROS body is reduced, so that increased expression levels of HIF, SOD, CAT levels were not significantly increased.