| * 投稿摘要： |
Pulmonary fibrosis in the lung tissue inflammation, alveolar be replaced by fibrous material originally soft as a sponge lung tissue becomes hard as concrete, and the gradual loss of the ability of gas exchange .Pulmonary fibrosis produced by organizational changes, including impaired alveolar septa, proliferation of lung parenchyma fibroblast cells and lung myofibroblasts, abnormal regeneration of the epithelial cells, and excessive deposition of extracellular matrix , in the process of pulmonary fibrosis, the cytokine excess production, and some cytokines will increase the collagen deposition, Some cytokines are reduced and also cause the release of various cytokines such as TNF-α,TGF-β, IL-6. TGF-β overexpression will induce fibroblast proliferation and collagen deposition,and important mediators in the injured tissue repair process and fibrosis. TGF-β itself is also involved in cell proliferation, fibrosis, tissue repair, inflammation, apoptosis, cell differentiation, cell adhesion and cell motility.Andrographolide(Andro) is isolated from a traditional Chinese herbal medicine. In recent years study,Andro can protective and choleretic, anti-inflammatory, antiviral, and increased glucose metabolism slow down diabetes, inhibition of platelet aggregation treatment of cardiac thrombus formation, has antioxidant, anti-cancer efficacy.but in the antifibrotic were few studies. so we choose one of A549 cells by adding TGF-β causes cells to produce fibrosis, and then stimulate the 3 different doses of the Andro. observation of collagen fibrosis of the subject and the capase family (cytochrom-c, capase 9, capase 3, capase 7,PARP) apoptosis signaling pathway, to discuss Andro reduce fibrosis lead to anti-apoptotic mechanism. The results indicate,Andro-reduced collagen, cytochrom-c, capase 9, capase 3, capase 7, PARP,so Andro maybe can reduce the effectiveness of pulmonary fibrosis.In the future may provide new targets of anti-pulmonary fibrosis drug development. |
2025 年 07 月
