The preventive role of rifaximin in fructose induced nephrotoxicity

In recent years increased fructose consumption; has been associated with increased prevalence of metabolic syndrome that characterized by obesity, insulin resistance, dyslipidemia and hypertension. In the studies, with the purchase of fructose; glomerular hypertension, renal inflammation and tubulointerstitial damage and nephrotoxicity reported. Giving a long time fructose causes an increase in kidney weight. Firstly, focal tubular damage especially in the proximal tubules, tubular hyperplasia and proliferation develops. Fructose intake causes an increase in inflammatory pathway. Rifaximin is an antibiotic which has minimal systemic effects and it is not absorbed from gastrointestinal tract. Rifaximin has been found effective. Rifaximin has been found effective in hepatic encephalopathy and recently in the treatment of irritable bowel syndrome. Rifaximin is effective by inhibiting bacterial translocation and making bacterial decontamination. In this study we aimed to investigate the preventive role of rifaximin in an experimental model of nephrotoxicity that created with fructose. A total of 42 male Sprague-Dawley rats were used in this study. The rats were divided into 6 groups of equal number : Group 1 (n=7) : Normal diet was given for 8 weeks, Group 2 (n=7) : High-fructose diet (30% fructose to be added to drinking water) was given for 8 weeks, Group 3 (n=7) : High fructose diet + once a week rifaximin with orogastric sonde for 8 weeks, Group 4 (n = 7), 3 days a week rifaximin with orogastric sonde for 8 weeks, Group 5 (n=7) : Normal diet + once a week rifaximin with orogastric sonde for 8 weeks, Group 6 (n=7) 3 days a week rifaximin with orogastric sonde for 8 weeks was given (Rifaximin 15 mg / kg dose administered). High-fructose diet histologically induced tubular dilatation and hydropic degeneration in the epitelium of tubule, caused a decrease in glomerular size. While there was no significant difference in serum urea and creatinine, uric acid levels increased intake of fructose. The dose-dependent rifaximin simultaneously, turning back to tubular and glomerular changes and decreased uric acid levels. Significant increase in tissue levels of malondialdehyde (MDA),TNF-α and NF-κB was observed in rats feeded with fructose rich diet (p<0.05). This increase was significantly decreased dose-dependently with added rifaximin to this diet (p<0.05). A significant decrease in tissue levels of Nrf-2, CAT, SOD, HO-1, GSP-x and GSH was observed in rats feeded with fructose rich diet compared to control group (p<0.05). This decrease was significantly increased döşe-dependently with added rifaximin to this diet (p<0.05). Our data showed that fructose causes oxidative stress and kidney injury. In conclusion, we determined that rifaximin can prevent fructose induced nephrotoxicity.