ABSTRACT
Bronchopulmonary dysplasia is one of the common complications related to premature infants. It is one of the main causes of disability or death in premature infants. There is still lack of specific prevention and treatment measures. In recent years, molecular biology studies have found that micro-RNA plays an important role in the occurrence and development of bronchopulmonary dysplasia. In this paper,the research of micro-RNA in the pathogenesis of bronchopulmonary dysplasia is reviewed,and the theoretical basis is laid for the search for new diagnosis and treatment methods.
ABSTRACT
There are growing evidences that pinocembrin has better neuroprotective effect. In the present study, the effect of pinocembrin on mitochondrial respiratory function was evaluated in global brain ischemia/ reperfusion (4-vessel occlusion, 4-VO) rats. The results showed that pinocembrin improved the respiratory activity of 4-VO brain mitochondria, through increasing ADP/O, state 3 respiration state (V3), respiration control rate index (RCI) and oxidative phosphorylation rate (OPR). And then, the effect of pinocembrin on brain mitochondria was verified in vitro. The results showed that pinocembrin increased ADP/O, state 3 respiration state, respiration control rate index, oxidative phosphorylation rate in NADH/FADH2 dependent respiratory chain and decreased state 4 respiration state (V4) in NADH dependent respiratory chain. Pinocembrin improved ATP content in brain mitochondria in vitro and in SH-SY5Y cells.
Subject(s)
Animals , Male , Rats , Adenosine Diphosphate , Metabolism , Adenosine Triphosphate , Brain Ischemia , Pathology , Cell Line, Tumor , Cell Respiration , Flavanones , Pharmacology , Hippocampus , Pathology , Mitochondria , Physiology , Neuroblastoma , Metabolism , Pathology , Neurons , Neuroprotective Agents , Pharmacology , Oxygen , Metabolism , Rats, Sprague-DawleyABSTRACT
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.