Fucosylated chondroitin sulfate attenuates renal fibrosis in animals submitted to unilateral ureteral obstruction: a P-selectin-mediated event?

Fibrosis is the end point of most renal diseases, and several glycosaminoglycans have been shown to attenuate this process. Marine invertebrate glycosaminoglycans with unique structures have opened the possibility to test these new compounds on renal fibrosis. The effect of a fucosylated chondroitin sulfate from an echinoderm marine species is reported with the use of a model of renal fibrosis in rats, termed unilateral ureteral obstruction.

Experimentally induced metabolic acidosis in rabbits modulates the interaction of aortic glycosaminoglycan with plasma low-density lipoprotein--an interesting observation about the association of acidosis and atherosclerosis.

It is well established that arterial glycosaminoglycans (GAG) undergo compositional and structural modifications during the development of atherosclerosis. On the other hand, metabolic acidosis is a common feature of chronic renal patients known to present accelerated atherogenesis. The present study was performed to determine the influence of acidosis in the modifications of aortic GAG in a model of atherosclerosis in rabbits.

Effects of molecular size and chemical structure on renal and hepatic removal of exogenously administered chondroitin sulfate in rats.

Chondroitin sulfate, a glycosaminoglycan that is widely distributed among mammals, is used as a therapeutic agent in various diseases. Here, we focus on its absorption, excretion and tissue accumulation in rats. The concentration of 35S-chondroitin sulfate (35S-CS) in plasma reaches a peak in the first 5 min after intravenous administration and simultaneously increases in the urine.