en Medical Biotechnology Medical Biotechnology مقاله کامل Full Length/Original Article <strong>Background</strong>: Hyperuricemia induces nephropathy through the mediation of oxidative stress, tubular injury, inflammation, and fibrosis. The high uric acid level is associated with the reduction of vitamin D levels. However, the reno-protective effects of this vitamin in hyperuricemia condition remain unknown. This study aimed to elucidate calcitriol treatment in a uric acid-induced hyperuricemia mice model. <strong>Methods</strong>: Uric acid (125 mg/kg <em>body weight</em> [BW]) was administered intraperitoneally for 7 (UA7) and 14 (UA14) days. Calcitriol (0.5 mg/kg BW) was intraperitoneally injected for the following seven days, after 14 days of uric acid induction (UA14VD7 group). The control group received NaCl 0.9%, by the same route. Serum creatinine was measured using calorimetric method, and uric acid levels were assessed using enzymatic calorimetric assay. Tubular injury and fibrosis were assessed using PAS and Sirius red staining. RT-PCR and real-time reverse transcription <em>PCR</em> were carried out for the analyses of <em>SOD-1</em>, <em>Collagen-</em>1, and <em>TGF-</em><em>b1 </em>mRNA expression in the kidney. Immunostaining of super oxide dismutase type 1 (SOD-1) was performed to detect its expression in the kidney. <strong>Results</strong>: Uric acid and creatinine levels markedly increased in UA14 groups, followed by an exacerbation of tubular injury. RT-PCR revealed the upregulation of <em>Collagen-1</em> and <em>TGF-</em><em>b1</em>, along with the downregulation of <em>SOD-1</em>. Calcitriol treatment attenuated the injury with reducing uric acid and creatinine levels, as well as tubular injury. This was associated with lower <em>Collagen-1</em> and <em>TGF-</em><em>b1</em> mRNA expression compared to the UA7 and UA14 groups. SOD-1 was upregulated in epithelial cells in the UA14VD7 group. <strong>Conclusion</strong>: Calcitriol treatment after uric acid induction may attenuate kidney injury through upregulation of <em>SOD-1</em> and downregulation of <em>Collagen-1</em> and <em>TGF-</em><em>b1</em> gene expression. Fibrosis, Hyperuricemia, Kidney injury, Superoxide dismutase-1, Vitamin D 417 425 http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-4028-2&slc_lang=en&sid=1 Muhammad Mansyur Romi romi.mm@ugm.ac.id 0000-0002-5842-9091 Yes Department of Anatomy Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia Nur Arfian nur_arfian@ugm.ac.id 0000-0003-1694-2054 No Department of Anatomy Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia Wiwit Ananda Wahyu Setyaningsih wiwit.ananda.w@ugm.ac.id 0000-0002-4334-5012 No Department of Anatomy Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia Rachma Greta Perdana Putri rachmagreta@gmail.com 0000-0002-6475-8473 No Department of Pathology, Faculty of Medicine, Universitas Ahamad Dahlan, Yogyakarta, Indonesia Mohammad Juffrie mjuffrie@ugm.ac.id 0000-0002-2862-3897 No Department of Pediatrics Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia Dwi Cahyani Ratna Sari dwi.cahyani@ugm.ac.id 0000-0002-1126-4939 No Department of Anatomy Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia