ABSTRACT
Chronic kidney disease (CKD) has emerged as a significant public health concern. In this article, we investigated the mechanism of oat dietary fiber in regulating CKD. Our findings indicated that the gut microbiota of CKD patients promoted gut microbiota dysbiosis and kidney injury in CKD mice. Intervention with oat-resistant starch prepared by ultrasonic combined enzymatic hydrolysis (ORSU) and oat ß-glucan with a molecular weight of 5 × 104 Da (OBGM) elevated the levels of short-chain fatty acids (SCFAs) and regulated gut dysbiosis in the gut-humanized CKD mice. ORSU and OBGM also reduced CKD-related uremic toxins such as creatinine, indoxyl sulfate (IS), and p-cresol sulfate (PCS) levels; reinforced the intestinal barrier function of the gut-humanized CKD mice; and mitigated renal inflammation and fibrosis via the NF-κB/TGF-ß pathway. Therefore, ORSU and OBGM might delay the progression of CKD by modulating the gut microbiota to reduce uremic toxins levels. Our results explain the mechanism of oat dietary fiber aimed at mitigating CKD.
ABSTRACT
OBJECTIVE: To investigate the preventive and therapeutic effects and the possible mechanisms of Dilingdan Decoction (DLDD), a compound Chinese herbal medicine, on rats with renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction (UUO). METHODS: Sixty SD rats were randomly divided into sham-operated group, untreated group, enalapril-treated group and DLDD-treated group. Blood urea nitrogen (BUN), serum creatinine (SCr), urine protein quantization in 24 hours and pathological changes of the obstructed kidney were observed. The expressions of transforming growth factor-beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA), fibronectin (FN) and laminin (LN) were detected by immunohistochemical method and colored-multimedia pathological image analysis system. RESULTS: Massive inflammatory infiltrates and collagen expression in renal interstitial in the untreated group were observed on the 7th day. Compared with the sham-operated group, percentages of area of TGF-beta1, alpha-SMA, FN and LN expressions in the untreated group were markedly increased (P<0.05), while the percentage of area of interstitial fibrosis was decreased in the DLDD-treated group as compared with the untreated group (P<0.05). On the 14th day, the percentages of area of TGF-beta1, alpha-SMA, FN and LN expressions were declined in two treated groups as compared with the untreated group (P<0.05), but had no statistical difference in biochemical indicators, including BUN, SCr and 24-hour urinary protein. On the 21st day, the level of SCr and the percentage of area of TGF-beta1 expression in the DLDD-treated group were lower than those of the enalapril-treated group (P<0.05). CONCLUSION: DLDD can reduce the excretion of urinary protein and the degree of interstitial fibrosis, and significantly inhibit the expressions of TGF-beta1, alpha-SMA, FN and LN. DLDD is superior to enalapril in protecting renal function after long-time application in rats.
