| 논문분류 | 춘계학술대회 초록집 |
|---|---|
| 제목 | Probiotics attenuate chronic kidney disease progression in mice |
| 저자 | Jihyun Yang*, Myung-Gyu Kim, Young Ju Na, Sung Yoon Lim, Won-Yong Cho, Sang-Kyung Jo |
| 출판정보 | 2016; 2016(1): |
| 키워드 | renal failure: chronic, progression of renal disease, treatment |
| 초록 | Background: Emerging evidence showed the important role of kidney-gut crosstalk in diverse pathological processes and alterations in intestinal barrier or dysbiotic gut microbiota have been demonstrated in chronic kidney disease (CKD). Regulatory T cells (Tregs) are known to be important in maintaining immune homeostasis in various inflammatory diseases and recent several in-vitro experiments demonstrated that probiotics could induce an expansion of Tregs. The purpose of this study was to investigate the effect of probiotic treatment on the CKD. Methods: CKD was induced in 6 week old C56BL/6 mouse by 5/6 nephrectomy. Lactobacillus Rhamnosus R0011 and Lactobacillus Acidophilus R0052 and proton pump inhibitor mixture were administered via oral gavage starting 1 day after the operation and continued for 8 weeks following intestinal decontamination. Biochemical, histological analyses as well as immunological analyses were performed at 4 weeks after 5/6 nephrectomy. Results: At 8 weeks, serum creatinine decreased in probiotics treated group compared to CKD group and sham operated mice (p=0.03). Probiotics group shows decreased fibrosis in MT stain semi quantification (p=0.05). Urine protein creatinine ratio showed no statistical significance but we confirmed the declining trend in probiotics group (p=0.13). This beneficial effect was associated with significant increased percentage of colonic FoxP3 (p=0.03). Serum IL-6 concentration was remarkably lower in probiotics group (p=0.02). Kidney TNF-α and MCP-1 concentration was higher in CKD group (p<0.01). Probiotics conjugate intestinal condition which is responsible for anti-fibrotic mechanism. Conclusion: Probiotics have renoprotective effect by reducing renal fibrosis through kidney-gut crosstalk and inhibit CKD progression. |
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