The Effect Of “supporting Kidney To Eliminate Turbid” On Progressing Tubulointerstitial Damage In MsPGN Rat

ObjectiveMesangial proliferative glomerulonephritis(MsPGN) in tubulointerstitial kidney injury is one of the main factors for end-stage development, is also chronic kidney disease(CKD) in the main types of renal failure in China. Its occurrence and development is determined by inflammatory cells, produce cytokine activation, the cells inherent phenotypic change, ECM accumulation and other factors. At present,the mechanism of renal tubulointerstitial damage is not very clear. In the treatment of Western medicine, there is no reliable therapy, many drugs are only stay in the stage of laboratory research. Therefore, in exploring aspects of drug,search for effective drug toxic side effects is particularly important. This study collected MsPGN tubulointerstitial injury pathological model, BSA rats fed every two days, intravenous injection of SEB, regular subcutaneous intramuscular injection of Freund’s adjuvan, copy rat mesangial proliferative glomerulonephritis model, and extend the modeling time to a stage tubulointerstitial damage. fushenJiangzhuo treaed MsPGN and observed on renal tubular interstitial injury cytokine TGF-β1, CTGF, COLⅢ and AngⅡ, and collagen synthesis, cell proliferation, tubular epithelial phenotype transformation and EMC interaction between generated. The clinical application of the drug for the treatment of tubulointerstitial injury provides a scientific basis. Method1, establish the system model of mesangial proliferative glomerulonephritis rats, to extend the modeling time to develop to renal tubulointerstitial injury.2, the male Wister rats were randomly divided into normal group, model group, Chinese medicine group and Western medicine group. Each group is 10 rats. Traditional C hinese medicine group and Western medicine group rats in drug intervention group was given modeling drug intervention.At the same time, traditional C hinese medicine was given with fushenjiangzhuo, dose per gram powder containing crude drug 4.06 g, western medicine group was given with benazepril, the dose of 1.8mg/kg. The two groups were given once a day, using 16 weeks.3, Observing the general condition, 24 h urinary protein, serum creatinine of rats in each group(Scr), blood urea nitrogen(BUN), the pathological changes of renal tissue in microscope, and the difference of descending the turbid, invigorate the kidney and benazepril on renal function in renal tubulointerstitial injury in rats.4, In the renal tissue, immunofluorescence staining labeled observation expression TGF-β1, CTGF; renal histological changes were observed in renal fibrosis and tissue factor on morphology and ultrastructure damage.5, through the expression of immunofluorescence staining method for the detection of AngII, to investigate the FushenJiangzhuo method of renin angiotensin system.6, immunohistochemical was measured in renal interstitial COLⅢ protein content, and to explore fushenJiangzhuo method of excessive accumulation of cell matrix protein on renal fibrosis. Result1. In the improvement of renal function: kidney and urine can reduce 24 h urine protein, BUN and Scr levels in rats.2. The improvement in fibrosis formation: Fushen Jiangzhuo prescription may be through inhibiting the expression of TGF beta 1 and downstream CTGF, and delay the development of renal interstitial fibrosis; regulating the expression of col III, AngII, inhibit excessive accumulation of ECM. This experiment also confirmed that TGF- beta 1 had correlation with C TGF and AngII3. To improve the pathological morphological changes: under light microscope, model group, glomerular hypertrophy, mesangial cells and matrix in the moderate to severe diffuse hyperplasia, renal tubular epithelial cells, edema, luminal stenosis, interstitial inflammatory cell infiltration, and the capillary pressure is obvious. Tip model replication success. Medication group, the renal tubular atrophy, inflammatory cell infiltration, increase of EMC and tubular atrophy levels were significantly lighter in the pathologic model group and compared with benazepril group, Fushen Jiangzhuo group, pathological changes of lighter. ConclusionThe experimental shows that: FushenJiangzhuo can improve renal function, reduce the pathological damage of kidney tissue; can effectively inhibit MsPGN rat renal tubular atrophy, interstitial infiltration of inflammatory cells, extracellular matrix increased, and improve the degree of renal tubulointerstitial damage, and its mechanism may be related to reduced renal interstitial TGF- β1, CTGF and COLⅢ; regulation of secretion of renin- angiotensin system. The experimental results indicated that: the treatment of turbid Decoction on MsPGN, possibly through inhibition of fibrosis factor gene expression and interaction between the genera tion, the regulation of the extracellular matrix, protect the renal tubular interstitial damage, improve renal function, and delay the progression of renal fibrosis.