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At least 1,513 records · Page 84Linked to original sources
PubMed2004

[Preventive and therapeutic effects of astragalus and angelica mixture on renal tubulointerstitial fibrosis after unilateral ureteral obstruction in rats].

OBJECTIVE: To investigate the preventive and therapeutic effects of Astragalus and Angelica mixture A&A on renal tubulointerstitial fibrosis after unilateral ureteral obstruction UUO in rats and their mechanisms. METHODS: UUO rats were randomly divided into Sham, UUO, A&A or ACEI groups. A&A, ACEI or the same amount of water was administered by gavage beginning 24 hours before UUO preparation and continued through ten days after UUO. Sera and the kidney tissues were collected from each group on the tenth day. Scr and BUN were measured. Trichrome staining, measurement of tubulo interstitial damage index and immunohistochemical studies localizing alpha-smooth muscle actin alpha-SMA , TGF-beta1, fibronectin FN , laminin LN were carried out. RESULTS: In UUO rats, the tubular-interstitial damage index, the expressions of alpha-SMA, TGF-beta1, FN and LN were all increased compared with those of Sham group. The tubulo interstitial damage index had positive correlation with expressions of alpha-SMA, TGF-beta1, FN and LN. A&A significantly ameliorated deterioration of renal function, tubulo interstitial damage index and inhibited the over-expressions of alpha-SMA, TGF-beta1, FN and LN in UUO rats. These anti-fibrotic effects were similar to those affected by ACEI. CONCLUSION: In renal interstitial fibrosis-induced UUO rats, A&A retard the progression of renal fibrosis and renal function deterioration by inhibiting myofibroblasts and suppressing TGF-beta1 expression, which may consequently result in a decreased production of extracellular matrix.

Angelica↗
PubMed2004

[Secondary nephrotic syndrome due to cardiovascular disease].

Cardiovascular diseases ralely evoke nephrotic syndrome. Especially hypertensive renal disease (nephroscrelosis) and renovascular hypertension occasionally may lead to nephrotic syndrome. We reported a case of nephrotic syndrome with renovascular hypertension successfully treated with candesartan. In eldery patients cardiovascular diseases are appeared. It is very important for clinicians to detect the mechanism of nephrotic syndrome caused by cardiovascular diseases.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

[Ischemic renal disease: revascularization or conservative treatment?].

Ischemic nephropathy is recognized as a distinct cause of renal insufficiency and it is defined as a significant reduction in glomerular filtration rate in patients with hemodynamically significant renovascular occlusive disease. We argue the epidemiologic and clinical manifestations of atherosclerotic renovascular disease, and we evaluate the pronostic agents. Published studies of the outcome of revascularization for renal-artery stenosis have been excellent, offering a durable patency and functional improvement but they have had numerous limitations. The atherosclerosis is a systemic disease and it provides the general prognosis of patients. We conclude that ischemic renal disease is a nephropathy of smoker men, with proteinuria excretion similar to nephropathy with unilateral stenosis. The age of patients is the clinical feature that decide the treatment: surgery, angioplasty/stent or medical management. Comparative analysis of percutaneous transluminal angioplasty and operation for renal revascularization and medically treated patients have proved that the advanced chronic renal insufficiency is associated with an unfavourable response of treatment of the ischemic nephropathy. But, in this nephropathy the revascularization can be the better therapy for selected patients. The revascularization with angioplasty/stent for patients with unilateral renal stenosis and chronic renal insufficiency has a doubtful effectiveness, as the chronic renal failure is result of nephroangiosclerosis.

Adult↗
PubMed2004

[Expression of p27 in renal interstital fibrosis in rats induced by unilateral ureteral obstruction].

OBJECTIVE: To explore the role of p27 in the renal tubule on the process of renal interstitial fibrosis caused by unilateral ureteral obstruction (UUO) in rats. METHODS: Rats were killed at the 7th, 14th, 21st days after UUO or sham-surgery. The protein expression of p27 in renal tubule was detected by immuohistochemistry at each time point. RESULTS: At the 7th day after the surgery, no noticeable abnormalities of p27 expression were found in renal tubular cells between UUO and the sham operated surgery. At the 14th and 21st days after UUO, the p27 expressions in renal tubular cells obviously decreased compared with those after the sham operated surgery. CONCLUSION: The p27 expression has no noticeable changes in the early UUO rats, and then it was significantly reduced with the renal interstitial fibrosis progressing.

Animals↗
PubMed2004

[Effect of perindopril on renal interstitial fibrosis of hypertension in rats].

OBJECTIVE: To explore the effect of perindopril on renal interstitial fibrosis of spontaneously hypertensive rats and on the expression of transforming growth factor-beta1. METHODS: Spontaneously hypertensive rats at the age of 9 weeks were randomly assigned to 2 groups: Spontaneously hypertensive rats (SHR, vehicle once daily, n = 10) and Treament-SHR (T-SHR, perindopril, 4 mg/(kg x d), per day PO, n = 10). Wistar-Kyoto rats (WKY, n = 7) were served as controls. After 10 weeks of treatment, the serum concentration of TGF-beta1, collagen type I, III and TGF-beta1 in the renal interstitum and renal mRNA levels of TGF-beta1 were detected. RESULTS: There were no significant differences in the serum TGF-beta1 levels among the 3 groups (P > 0.05). Immunohistochemical studies revealed a significant interstitial accumulation of collagens I, III and TGF-beta1 in SHR compared with those in WKY (P < 0.01 or P < 0.05). These changes in SHR were significantly ameliorated by the administration of perindopril (P < 0.01 or P < 0.05). In SHR, renal TGF-beta1 mRNA expression was increased significantly compared with that in WKY (P < 0.01), but perindopril decreased it to the normal levels of WKY (P > 0.05). The increased expression of TGF-beta1 was blocked by perindopril. The expressions of collagens I and III in renal interstitum significantly correlated with the accumulation of TGF-beta1 in the renal (r = 0. 734, r = 0.762, respectively; P < 0.01). CONCLUSION: The tubulointerstitial fibrosis of spontaneously hypertensive rats is mediated by an increased level of TGF-beta1 in the renal tissue, and perindopril may decrease the expression of TGF-beta1 to ameliorate the tubulointerstitial fibrosis.

Angiotensin-Converting Enzyme Inhibitors↗