An oral absorbent, surface-deacetylated chitin nano-fiber ameliorates renal injury and oxidative stress in 5/6 nephrectomized rats. (1st April 2017)

• Record Type: Journal Article
• Authors: Anraku, Makoto; Tabuchi, Ryo; Ifuku, Shinsuke; Nagae, Tomone; Iohara, Daisuke; Tomida, Hisao; Uekama, Kaneto; Maruyama, Toru; Miyamura, Shigeyuki; Hirayama, Fumitoshi; Otagiri, Masaki
• Is Part Of: Carbohydrate polymers. Volume 161(2017)
• Page Start: 21
• Page End: 25
• Publication Date: 2017-04-01
• Subjects: Surface-deacetylated chitin nano-fiber -- Antioxidant -- Renal failure -- Oxidative stress -- Adsorption; Polysaccharides -- Periodicals; Polysaccharides -- Periodicals; Polysaccharides -- Périodiques; Electronic journals; 547.78
• DOI: 10.1016/j.carbpol.2016.12.057
• Languages: English
• ISSNs: 0144-8617

Abstract

Highlights: The effect of SDACNFs on oxidative stress was examined in CRF model rats. A low-dose of SDACNFs results in a reduction of uremia. A low-dose of SDACNFs decreases the levels of uremic toxins. The level of oxidative stress is correlated with serum indoxyl sulfate levels. A low-dose of SDACNFs might result in a decreased cardiovascular disease. Abstract: In this study, we report that surface-deacetylated chitin nano-fibers (SDACNFs) are more effective in decreasing renal injury and oxidative stress than deacetylated chitin powder (DAC) in 5/6 nephrectomized rats. An oral administration of low doses of SDACNFs (40 mg/kg/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 DAC or AST-120. The SDACNFs treatment also resulted in an increase in antioxidant potential, compared with that for DAC or AST-120. Immunohistochemical analyses also demonstrated that SDACNFs treated CRF rats showed a decrease in the amount of accumulated 8-OHdG compared with the CRF group. These results suggest that the ingestion of SDCH-NF results in a significant reduction in the levels of pro-oxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation.