Heparin is an anticoagulant activity of free Irbesartan Avapro soldering and pro-angiogenic. The effectiveness of SST0001 by removing the biological activity t of heparanase in vivo in models of heparanase-au processes He DN, such as inflammation, tumor growth and metastasis demonstrated. To test the effect of inhibition of heparanase in DN, we used BALB / c mouse strain known to be particularly sensitive to DN. Diabetes was induced by multiple administrations lowdose STZ. Mice five days after the last administration of STZ, diabetic M Were divided into two groups and with SST0001 or vehicle. The blood glucose levels in experimental Mice were maintained with 300 mg / dl administered by treatment with 0.4 units of insulin every other day. As expected, 12 weeks after induction of diabetes, a significant increase of 24 h urinary albumin excretion in the urine of diabetic vehicle-treated BALB / c mice M Proven. Interestingly, the treatment has entered SST0001 Born a statistically significant decrease twice in 24 hours urine albumin excretion. The difference between 24 h albumin excretion in SST0001 treated compared to M Mice that were treated with vehicle during the 16th Week of the experiment as well maintained, although it did not reach statistical significance. In addition, treatment assessment of renal function in diabetic M Mice experimentally vehicle at week 16 mice showed a significant increase in serum creatinine and blood urea nitrogen in relation to the health of non-diabetic M, W While in SST0001 M use treated diabetics, the corresponding values are not significantly different in diabetic compared with the M mice increased ht. In a similar manner, treatment with SST0001 in duplicate or greater Erer decline in 24 h urinary albumin excretion in the other two in vivo experimental systems: STZ-induced type 1 DN in DBA 2 Mice that with BALB / c strain is considered as one of the platforms are very useful for the modeling of DN and ADIP sen type 2 DN in db / db M mice, considered one of the best models of the genetic diabetic kidney disease, also to examine heparanase inhibition as a therapeutic approach m was like in DN.
Diabetes and its complications represent one of the most important health problems worldwide, which will probably various rfen to a critical level in the coming decades. DN is therefore an important medical concern. Thus, more data on the identity t of the downstream effectors are responsible for the pathogenesis of DN, which treats the correct treatment of the disease. Considerable progress has been made in deciphering the r The signaling pathways leading to more kidney damage Ending in diabetics. Conna is t minus r The exact ECM-degrading enzymes in the pathophysiology of DN. We demonstrate for the first time the significant involvement of heparanase in experimental DN and describe a molecular mechanism of induction of heparanase in hyperglycemia Mixing conditions. Despite the lack of direct experimental data for the Best Account the r The causal heparanase in the pathogenesis of DN have multiple reports an m Adjusted association between heparanase and DN analyzed. In addition, a relationship between heparanase and DN progression was been made in recent publications in question, against the participation of the enzyme in diabetic nephropathy. against the background of this controversy, the latest production offered heparanasenull of a mouse.