| Renal interstitial fibrosis is a common consequence of progressive renal diseases.As renal fibrotic changes well correlate with the reduction of glomerular filtration rate in the chronic renal diseases, renal fibrosis isbelieved to play a crucial role in the progression of chronic renal diseases.Renal tubulointerstitial injury is characterized by inflammatory cellinfiltrate:however,the stimuli for leukocyte recruitment are not fully understood.Several studies have demonstrated the importance of proinflammatory factors such as cytokines, adhesion molecules,growth factors,and vasoactive peptides in the progression of renal damage.Although the mechanisms leading to end-stage renal failure are not completely elucidated,It is well known that nuclear factor-kB ( NF-kB ) plays a pivotal role in many inflammatory diseases including renal disease.NF - kB proteins normally exist in the cytosol as dimers bound to inhibitory proteins ( IkB ):after exposure to different stimuli, IkB undergoes proteolysis,allowing NFkB to enter the nucleus and activate genes encoding chemokines and other proteins.Independently of the underlying renal disease,tubulointerstitial renal damage correlates best with the loss of renal function and the risk of progression to end-stage renal failure.Resident renal cells,such as tubular epithelial cells ( TECs ) ,might have an important role in the tubulointerstitial inflammatory process observed in many renal diseases.TECs,once considered passive bystanders in the disease process,have been shown to be actively involved being a rich source of cytokines,chemokines,and others inflammatory mediators.Human TECs in vitro produce large amounts of cytokinesIL-6 and TNF- α ,chemokines IL-8,MCP-l,and adhesion moleculesICAM-1,VCAM-1.Elevated levels of cytokines and chemokines have been documented in both resident renal cells and infiltrating inflammatory cells invarious forms of glomerulonephritis and tubulointerstitial nephritis and have been suggested to contribute to progressive renal failure in vivo.At present,the precaution of renal interstitinal fibrosis is increasingly being attatched importance to .the durg of adhesion molecule is only applied in laboratory but in clinic.Clinically proven strategies to slow progression of renal disease include: Blood pressure reduction ,protein restriction.Compared with the west medicine,lots of study indicate tradition medicine on renal fibrosis have better clinical effect and lower ill effect.Compound Biejia Ruangan Prescription ( CBRP ) ,consisting of eleven components as Rhizoma Atractylodis,Pericarpium Citri reticulatea,Ginger prepared Cortex Magnoiiae officinalis,Radix Angelicae dahuricae,Poria,Pericarpium Arecae,Rhiaoma Pinellia,Extractum Glycyrrhizae,Oleum Agastaches and Oleum Folii Perillae,has the function of promoting blood circulation and eliminating blood stasis,dissipating phlegm and dispersing goiter, replenishing Qi and nourishing Yin,and clearing away heat and removing toxic substances,et al.To discuss the preventing and treating effect of CBRP on Renal interstitial fibrosis,rat model induced by Unilateral ureteral occlusion in rats was adopted.This thesis describes the effect and mechanisms of CBRP on RIF from aspects of in vitro and in vivo level,which can provides experimental foundation for more exact and scientific therapy.The main contents and results are as follows: 1.Experimental study on the effect of CBRP on RIF.Investigation on physiology of Unilateral Ureteral Congestion affect renal interstitial fibrosis occurs and therapeutic effect of CBRP on RIF.105 male Wistar rats,weighting 200±20g,adopted for a week.All rats except normal group,sham-operated rats underwent unilateral ureteral obstruction, inhibition,rats were divided into 7 groups as follows-.normal group,sham-operation group,model control group,positive medicine group,and high,moderate and low CBP groups.From the day after modeling,CBRP solution of different dosages ( 1.4g/kg 0.7g/kg 0.35g/kg ) was given to rats in the high,moderate and low CBP group by...
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