An Experimental Research That Beryllium Oxide Induced Lung Injury And The Protective Effects Of LBP In Rats

Objective This study established animal m Ael, after exposure by detecting lung lavage and lung tissue homogenates of superoxide dismutase(SOD) activity, malondialdehyde(MDA), nitric oxide synthase(NOS) activity, nitric oxide(NO) content and glutathione peroxidase(GSH-Px) activity,lung tissue oxidative damage associated gene thioredoxin(TRX), hypoxia-inducible factor-1(HIF-1),vascular endothelial growth factor(VGEF), and heme oxygenase(HO-l) expression, lung Histopathological changes in the light microscopy and electron microscope, exploring the pathogenesis of beryllium compounds induced lung injury.Studies in experimental animals will also join the Lycium barbarum polysaccharides(LBP) to intervene, investigate the protective effect induced lung injury process which occurs in beryllium compounds, providing a new way for early occupational contact beryllium lung injury prevention.Methods 128 SPF grade male SD rats, after adaptive feeding randomly divided into control group(8), the saline group(24), Be O exposure group(32), Be O + LBP low-dose group(32), Be O + LBP high-dose group(32). Intratracheal a perfusion Be O suspension 0.5ml, saline injected the same amount of sterile saline, was exposed next to Be O + LBP low-dose group, Be O + LBP LBP fed high-dose group. Points 20 d, 40 d, 60 d and 80 d four dead rats get along, were the following experiment:1.Take the same position on the right lung tissue, making lung tissue pathology, microscopy. Take the same parts of the right middle lobe 1 × 1 × 1mm3 organization, observed under transmission electron microscope.2. Take the left lung lavage preparation, leaves the same site preparation lung homogenates of lung tissue kit lung lavage and lung tissue homogenates of superoxide dismutase(SOD) activity, malondialdehyde(MDA), nitric oxide synthase(NOS) activity, nitric oxide(NO) content and glutathione peroxidase(GSH-Px) activity. 3.ELISA detect lung tissue oxidative damage related genes TRX, HIF-1, VGEF, and HO-l protein expression.Results(1) Anatomical observation: each time the surface of the lung tissue of rats in contrast to pink, soft and smooth touch. Early exposure to the visible surface of the lung congestion, lung tissue volume increases, the surface of the cyst, white miliary n Aules. Post-exposure, lung tissue surface white, covered the whole lung n Aules, the integrity of lung tissue atrophy, touch harden. After LBP intervention group compared with the exposure, each time alleviate the pathological changes. Light microscopy: when contrasted each morphologically normal lung tissue. Early exposure mainly as interstitial pneumonia, interstitial lung, bronchial and alveolar epithelial wall a lot of inflammatory cell infiltration. Post-exposure lung tissue consolidation, pulmonary artery atherosclerosis occurs, terminal bronchioles pseudostratified ciliated columnar epithelium formed the axis of papillary hyperplasia. Electron microscope observation: each time in contrast to normal lung tissue ultrastructure. Early exposure of alveolar epithelial cells type ? part osmiophilic b Aies appeared emptying phenomenon, endothelial cell proliferation. Mitochondrial electron density increased, smooth endoplasmic reticulum was dilated. Post-exposure osmiophilic b Aies basically empty, mitochondria cavitation increase, chromatin condensation, microvilli. LBP after the intervention, compared with the exposed group, the pathological changes in the lung tissue of rats each time there is a certain degree of relief.(2) Be O exposure 60 d, after 80 d, and while contrast group, the lung tissue homogenates, bronchoalveolar lavage fluid SOD, NOS activity, NO content reduced, GSH-Px activity, MDA content increased, and difference was statistically significant(P <0.05 or P <0.01). LBP intervention 60 d, after 80 d, compared with Be O exposure group, lung tissue homogenates, bronchoalveolar lavage fluid SOD, NOS activity, NO levels increased, GSH-Px activity decreased, LBP in the high dose group 80 d the difference was statistically significant(P <0.05 or P <0.01). MDA content decreased, MDA content in 60 d, 80 d difference was statistically significant(P <0.05 or P <0.01) homogenates. LBP high dose group and low-dose group, SOD, NOS activity, NO levels increased, GSH-Px activity, MDA content decreased, lavage fluid NOS, GSH-Px activity, NO content 80 d difference was statistically significant(P <0.05 or P <0.01), MDA content in homogenates 60 d, 80 d difference was statistically significant(P <0.05 or P <0.01).(3)After Be O exposure, 40 d Be O exposure group, LBP low-dose group and the control group, HO-1 content increased, 80 d Be O exposure, LBP intervention group and the control group, HO-1 concentrations decreased, the difference were statistically significant(P <0.05 or P <0.01); 40 d Be O exposure group, LBP intervention group, 60 d, 80 d Be O exposure group HIF-1 level was higher, the difference was statistically significant(P <0.05 or P <0.01); VEGF levels increased each time, including 40 d, 80 d Be O exposure group, LBP intervention group, 60 d Be O exposure group compared with the control group, the difference was statistically significant(P <0.05 or P <0.01).TRX each time content increased compared with control group, the difference was statistically significant(P <0.05 or P <0.01).After the LBP intervention, HO-1 content of less than Be O exposure group 40 d, 80 d Be O higher exposure group, the differences were statistically significant(P <0.05); 60 d LBP high dose group, 80 d LBP low intervention group HIF-1 content in Be O exposure group, the difference was statistically significant(P <0.01); 40 d LBP intervention group, 80 d LBP high dose levels of VEGF and Be O relatively lower exposure group, the difference was statistically significant(P <0.05 or P <0.01).Conclusions(1) Be O can cause lung tissue damage, mainly in the early inflammatory tissue damage, with the extension of exposure time, the organizational changes in the structure and function of real change, hardening of the arteries, organelles destruction.(2) Be O can make antioxidant enzyme activity in vivo in rats abnormal changes, lipid peroxidation enhanced peroxidation products generated increased, causing oxidative damage to lung tissue.(3) Beryllium oxide causes oxidative damage related genes HIF-1, VGEF, HO-l and TRX expression abnormal, causing tissue damage.(4) LBP on tissue damage caused by beryllium oxide has a protective effect, this protective effect is by increasing the body's antioxidant levels to achieve.