Abstract
The administration of a high-molecular polysaccharide Sacran results in a significant decrease in renal injury and oxidative stress, compared with that for the oral carbonaceous adsorbent, AST-120 (Kremezin®) or a non-treatment group in 5/6 nephrectomized rats. An oral administration of Sacran (20 mg/day) over a 4 week period resulted in a significant decrease in serum indoxyl sulfate, creatinine and urea nitrogen levels, compared with a similar treatment with AST-120 or the non-treatment group. Sacran treatment also resulted in antioxidant potential being maintained, compared with that for AST-120 or the non-treatment group. Immuno-histochemical analyses also demonstrated that CRF rats, when treated with Sacran, showed a decrease in the level of accumulated renal fibrosis and 8-OHdG compared with AST-120 or the non-treatment group. These results suggest that the ingestion of Sacran results in a significant reduction in the levels of prooxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation.
Highlights
Oxidative stress is generally assumed to be closely related to the progression of Chronic Renal Failure (CRF) and the onset of various complications, including Cardiovascular Disease (CVD) [1,2]
Uremic toxins have been proposed as possible candidates, because they accumulate in CRF and a direct relationship exists between the redox properties of uremic toxins and their biological activity; it would be highly desirable to develop an understanding of the redox properties of uremic toxins, in terms of managing oxidative stress in CRF patients
We report on the effect of sacran on oxidative stress and CRF in 5/6 nephrectomized rats, compared with the effects of AST-120, in an attempt to better understand the potential role of Sacran as an antioxidant in the systemic circulation using a sensitive marker for protein oxidation [22,23]
Summary
Oxidative stress is generally assumed to be closely related to the progression of Chronic Renal Failure (CRF) and the onset of various complications, including Cardiovascular Disease (CVD) [1,2]. It has recently been proposed that several factors significantly contribute to the enhancement of oxidative stress observed in CRF. Uremic toxins have been proposed as possible candidates, because they accumulate in CRF and a direct relationship exists between the redox properties of uremic toxins and their biological activity; it would be highly desirable to develop an understanding of the redox properties of uremic toxins, in terms of managing oxidative stress in CRF patients. A uremic toxin, has been extensively investigated in this regard. It is derived from dietary protein, including tryptophan, and contains an indole ring. It is present at high levels in the serum of patients with CRF, and
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