Connective Tissue Growth Factor, Nuclear Transcription Factor In Diabetic Rat Lung And The Intervention Of Matrine

Background:Pulmonary fibrosis is a fatal diffuse interstitial lung disease with unknown cause, pathogenesis is unclear and the lack of treatment. A variety of factors can lead to pulmonary fibrosis. In recent years, the impact of diabetes on the lung gradually aroused our attention. However, whether diabetes can lead to pulmonary fibrosis has been reported rarely at home and abroad..As an intracellular signal transduction pathways of inflammation control center of the nuclear factor-KB plays an important role in diabet's lung disease. Now more and more reported in the literature of connective tissue growth factor and fibrosis of various tissues and organs are closely related. Recent years, research confirmed matrine in anti-liver and kidney fibrosis have a certain effect, but on its effect on pulmonary fibrosis, has not yet been reported.Objective:Study CTGF, NF-κB expression in diabetic lung and explore possible mechanisms of lung disease and for clinical drug therapy to find a new target. Materials and methods:Male SD rats were randomly divided into 3 groups:1. Control group; 2. Model group; 3. Matrine (15mg/kg) group. By intraperitoneal injecting streptozotocin establish diabetic model, matrine group injected intraperitoneally at a later matrine 5 weeks. The corresponding control group injected with doses of 0.9% saline. At 4 weeks and 6 weeks, real-time quantitative RT-PCR determinated the content of CTGF, detected by Western Blot the protein expression of NF-κB levels in the diabetic lung.Results:1. Pulmonary fibrosis occurs in diabetic rats.In the experiment 4 weeks and 6 weeks, diabetic rats under the microscope appear pulmonary alveolitis, pulmonary fibrosis, and fibrosis as the disease became clear,at 6 weeks increased lung index, lung coefficient model group and the normal group was significantly higher compared (P<0.05), suggesting that diabetes causes pulmonary fibrosis.2. CTGF, NF-κB expression in Model group was increased.Real-time quantitative RT-PCR found that diabetes increased the amount of model CTGFmRNA than the control group. Western-Blot analysis showed that in normal lung tissues have low levels of NF-κB/p65 expression, the formation of diabetic rat lung tissue at 4 weeks was significantly higher NF-κB/p65, reaching 4.4 in normal control group fold (P<0.01),6 weeks was 4.2 times (P<0.01).3. Matrine can inhibit the diabetic rat lung CTGF, NF-KB/p65 expression:6 weeks matrine group lung coefficient compared with model group decreased (P <0.05). Real-time quantitative RT-PCR detected 4 weeks, decreased the amount of matrine group CTGFmRNA compared with diabetic rats 22.6%(P<0.05), At 6 weeks decreased compared with diabetic rats 55.9%(P<0.01). Western-Blot analysis showed that 4 weeks and 6 weeks increased the amount of NF-KB/p65 matrine group than the control group, decreased compared with diabetic rats. Matrine inhibited to a certain extent, CTGF, NF-κB/p65 expression, reduce pulmonary fibrosis.Conclution:Diabetes can lead to lung injury and pulmonary fibrosis gradually formed in the diabetic lung with CTGF, NF-κB expression increased, matrine can reduce CTGF,NF-κB expression, reducing fibrosis.This pulmonary fibrosis may be associated with CTGF, NF-κB over-expression. Matrine may reduce pulmonary fibrosis.