RESUMO
Objective:To study the role of miRNA-15b and vascular endothelial growth factor (VEGF) in the pathogenesis of novel bronchopulmonary dysplasia (nBPD) in rats.Methods:A total of 100 newborn SD rats were randomly assigned into BPD group and control group with 50 rats in each group. The BPD group was placed in oxygen chamber with 60% oxygen concentration and the control group received atmospheric air. The morphological changes of lung tissues were observed on 1 d, 7 d, 14 d and 21 d and the radial alveolar counts (RAC) and alveolar septal thickness (AST) were measured. The expression of miR-15b was measured using real-time quantitative PCR and the expression of VEGF in lung tissue was examined using ELISA method.Results:With prolonged oxygen exposure, the lung tissue of the BPD group showed a decrease in the number of alveoli, a gradual loss of the normal structure of alveoli and a significant widening of the alveolar septum. On 7 d, 14 d and 21 d, RAC values [(6.19±0.29) vs. (6.86±0.92), (5.35±0.67) vs.(9.75±0.34), (3.96±0.45) vs. (10.04±0.52)] were significantly lower in the BPD group than the control group ( P<0.05). On 7 d, 14 d and 21 d,the levels of AST in BPD group were significantly higher than the control group [(6.87±0.41) μm vs. (6.43±0.31) μm, (8.94±0.25) μm vs. (5.36±0.26) μm, (9.61±0.30) μm vs. (4.55±0.32) μm] ( P<0.05). On 7 d, 14 d and 21 d,the miR-15b expression in BPD group were significantly higher than the control group [(1.12±0.11) vs. (0.84±0.09), (1.33±0.09) vs. (0.73±0.07), (1.66±0.15) vs. (0.45±0.10)] ( P<0.05).On 7 d, 14 d and 21 d, VEGF in BPD group were significantly lower than the control group [(10.89±1.67) pg/ml vs. (23.86±4.38) pg/ml, (8.75±1.28) pg/ml vs. (53.94±3.49) pg/ml, (4.66±1.12) pg/ml vs. (70.37±3.10) pg/ml] ( P<0.05). Conclusions:MiR-15b and VEGF may play a role in the development of nBPD.
RESUMO
The aim of this study is to investigate the effects of the metformin on the formation of hepatic fibrosis in type 2 diabetic rats and discuss its mechanism of liver-protecting activity. After SD rats were fed with high-fat and high-sucrose diet for four weeks, low-dose streptozotocin (STZ) was injected intraperitoneally to make the animal mode of type 2 diabetes. Then, all diabetic rats was fed with the high-fat diet and metformin (ig, 100 mg x kg(-1)) was given orally to metformin group for four months. After the last administration, fasting blood glucose was determined. The livers were removed to calculate the hepatic coefficient and to make HE and Picro acid-Sirius red staining, immunohistochemistry (alpha-SMA and TGFbeta1) and TUNEL staining in order to evaluate the effect of metformin on the hepatic fibrosis. The animal model of type 2 diabetes with hepatic fibrosis was successfully made. Metformin can significantly alleviate the lesions of hepatic steatosis and fibrosis, markedly reduce the expressions of alpha-SMA and TGFbeta1 in liver tissue of type 2 diabetic rats. However, TUNEL staining result suggested that metformin could not reduce apoptosis of hepatocytes. The results suggest that metformin can inhibit the formation of hepatic fibrosis in type 2 diabetes.