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Abstract
Purpose
Hyperuricemia is an independent risk factor for renal damage and can promote the progression of chronic kidney disease (CKD). In the present study, we employ a rat model to investigate the effects of rosiglitazone (RGTZ), a peroxisome proliferator-activated receptor-gamma agonist, on the development of hyperuricemic nephropathy (HN), and we elucidate the mechanisms involved.
Methods
An HN rat model was established by oral administration of a mixture of adenine and potassium oxonate daily for 3 weeks. Twenty-four rats were divided into 4 groups: sham treatment, sham treatment plus RGTZ, HN, and HN treated with RGTZ.
Results
Administration of RGTZ effectively preserved renal function, decreased urine microalbumin, and inhibited interstitial fibrosis and macrophage infiltration in a rat HN model. RGTZ treatment also inhibited TGF-β and NF-κB pathway activation, decreased expression of fibronectin, collagen I, α-SMA, vimentin, MCP-1, RANTES, TNF-α, and IL-1β, and increased E-cadherin expression in the kidneys of HN rats. Furthermore, RGTZ treatment preserved expression of OAT1 and OAT3 in the kidney of HN rats.
Conclusion
RGTZ attenuates the progression of HN through inhibiting TGF-β signaling, suppressing epithelial-to-mesenchymal transition, reducing inflammation, and lowering serum uric acid levels by preserving expression of urate transporters.
Acknowledgments
This work was supported by Risk factors and prediction model of chronic kidney disease caused by metabolic syndrome: A multicentric prospective cohort study clinical trial training project of Southern Medical University (LC2016PY047, 2016), the Science and Technique Program of Guangzhou (201604020015, 2015), the South Wisdom Valley Innovative Research Team Program (CXTD-004, 2014), and The National Natural Science Foundation of China (81873620).
Disclosure
Xin Wang and Jin Deng are co-first authors. The authors report no conflicts of interest in this work.