ctgf sirna质粒对uuo小鼠肾脏间质纤维化的影响word格式论文.docxVIP

优秀毕业论文 精品参考文献资料 Effect of CTGF siRNA plasmid on renal interstitial fibrosis in UUO mice ABSTRACT Objective: Renal interstitial fibrosis is a common pathway of the development of a variety of kidney disease to end-stage renal disease. Renal interstitial myofibroblasts is the important cells to produce interstitial extracellular matrix (extracellularmatrix, ECM). Transforming growth factor β1 (TGF-β1) is a recognized factor-induced fibrosis. It can activate the mechanisms of renal tubular epithelial cells to tubular epithelial - myofibroblast ransdifferentiation, and thus expression of α-smooth muscle actin (α-SMA), Synthesis Ⅰ, Ⅳ collagen (collagen Ⅰ and IV), fibronectin and other extracellular matrix components involved in the process of renal interstitial fibrosis. Alpha-smooth muscle actin (α-SMA) is a specific marker of the muscle fibroblast, and is a cytoskeletal protein. In addition to vascular smooth muscle in normal renal tissue, few expressed α-SMA. But the renal interstitial cell cytoplasm, the basal side of renal tubular epithelial cells, and some atrophic epithelial cells of the small tubes can express a-SMA when the renal occured interstitial fibrosis. CollagenⅠ is the main collagen, widespread in a variety of connective tissue. It plays an indispensable role in renal fibrosis development. Its over-expression is an important part of the formation of renal interstitial fibrosis. Connective tissue growth factor (CTGF) is a profibrotic activity of TGF-β downstream signaling media, and it stimulate cell proliferation and extracellular matrix formation of fibers in the kidney, and it has an important role of renal fibrosis. Inhibiting CTGF gene expression has clearly contributed to slow down the process of renal fibrosis, the effect of inhibiting its expression with conventional anti-fibrosis drugs is not satisfactory. RNAi technology can inhibit post-transcriptional expression of target genes. Its role is similar to gene knockout, gene expression, but not a