The Expression Of IL-8 And GSH In BALF And HDAC2 In Lung Of Smoke Exposure And Smoking Cessation Rats

BACKGROUNDChronic obstructive pulmonary disease (COPD), as a chronic inflammatory disease, characterized by unfully reversible airflow limitation, is connected with the harmful gases or harmful particles in the air. Because of its high morbidity and high mortality, COPD is currently the fourth leading cause of death in the world and is projected to rank the fifth as a worldwide burden of disease by 2020. No currently available treatments reduce the progression of COPD or suppress the inflammation in small airways and lung parenchyma. Cigarette smoking is a risk factor for the development of airway hyperresponsiveness and COPD, because cigarettes' smog has lots of oxidant, like NO. The interaction between oxidative stress and inflammation in the lung, promotes the occurrence and development of COPD. No currently available treatments can reduce the progression of COPD or suppress the inflammation in small airways and lung parenchyma. Occurrent domestic and international research on the mechanisms of COPD has not got an unified theory, but all believe that there is a close relationship with smoking. One group claims that smoking can stimulate alveolar macrophages secret multiple cytokines, as TNF-α, IL-8 and prolease, all can mediate airway inflammation and lung tissue damage in COPD. The other group says the high activity oxidant in smoking fogs can lead airway's inflammation and lung tissue's damage by increasing the body's oxidant load and membrane's peroxidation. There are dozens of researches on smoking damage, but research on smoking cessation is rare. My experiment is aim to investigate the expression of IL-8 and GSH in BALF and HDAC2 in lung tissue of smoking and smoking cessation rats, study the reason of COPD and provide some clinical ideas for the next step treatment of COPD.OBJECTIVETo study the expression of IL-8 and GSH in BALF and HDAC2 in lung of smoke exposure and smoking cessation ratsMETHODS50 SD rats were divided into five groups randomly: normal control group (group A), 1-month smoking group (group B,), 2-month smoking group (group C), 1-month smoking-cessation group(group D),2-month smoking-cessation group(group E).Group B rats were exposured to cigarettes for 1 month, C, D, E were exposured to cigarettes for 2 months. At 1 month, group B were sacrificed , at 2 month, group C were sacrificed, group D was smoking cessation for 1 month and group E for 2 months . Pathomorphological changes of the small airway were analyzed, Collect the cells in BALF, and then detect the levels of IL-8, GSH by ELISA. Study the HDAC2 in rats'lung tissue.RESULT(1)Compared with group A, the levels of IL-8 in group B, group C, group D, group E are increased (P<0.05), but smoking groups are higher than smoking-cessation groups. In smoking groups, group C is higher than group B. In smoking-cessation groups, group D is higher than group E.(2)Compared with group A, the levels of GSH in group C, group D, group E are decreased (P<0.05), but group A levels are higher than other groups. In smoking groups, group C is lower than group B. In smoking-cessation groups, group D is lower than group E.(3)Compared with group A, the levels of HDAC2 in group B, group C, group D, group E are decreased (P<0.05), but smoking groups levels are lower than smoking-cessation groups. In smoking groups, group C is lower than group B. In smoking-cessation groups, group D is lower than group E.CONCLUTION(1)It showed that smoke exposure can lead rats lung inflammation. It can decrease after quitting, but still can't back to normal.(2)It showed that smoke exposure can stimulate rats oxidation reaction. It can decrease after quitting, but still can't back to normal.(3)It showed that the levels of HDAC2 in rats'lung tissue will decrease after smoking exposure. It can recrease after quitting, but still can't back to normal.