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논문분류	춘계학술대회 초록집
제목	Omega-3 fatty acid mitigates mitochondrial dysfunction and modifies renal myostatin expression in adenine-induced uremic rats
저자	Yu In Jeong
출판정보	2024; 2024(1):
키워드
초록	Objectives: Mitochondrial dysfunction and inflammation play a central role in the progression of chronic kidney disease. Myostatin may be related to inflammation but renal myostatin expression is not clear. We aimed to investigate whether omega-3 fatty acids (FA) regulate mitochondrial dysfunction in adenine-induced uremic rats. We also tried to elucidate whether omega-3 FA on renal myostatin expression and renal mitochondrial morphology. Methods: Male Sprague-Dawley rats were fed diets containing 0.75% adenine and 2.5% protein for three weeks. Rats were randomly divided into four groups that were fed diets containing 2.5% protein and saline with cholecalciferol (3000 IU/kg/week) or omega-3 FA (300 mg/kg/day) with cholecalciferol by gastric gavage for two weeks: normal control, adenine control sacrificed at 3weeks, adenine control sacrificed at 5weeks, omega-3 FA group sacrificed at 5weeks. The renal expression of myostatin and mitochondrial mediators was examined by western blot analysis. Renal mitochondrial morphology was evaluated using transmission electron microscopy. Results: Compared to normal, serum creatinine in adenine control was increased and improved in the omega-3 FA group. Compared with normal, PGC-1α, SIRT1/3, and Nrf2 were down-regulated in adenine control. DRP-1 was up-regulated in adenine control and recovered with omega-3 FA supplementation for 2 weeks. PINK1, BNIP3, and NIX were down-regulated in adenine control and recovered in the omega-3 FA group. Compared to normal, renal myostatin expression was continuously downregulated at 3 weeks and 5 weeks and recovered with omega-3 FA. The size and number of tubular mitochondria were decreased at 5 weeks and mitigated with omega-3 FA supplementation for 2 weeks. Conclusions: Omega-3 FA is beneficial for mitochondrial dysfunction and morphology in uremic rats. Further studies are necessary to find the pathogenic mechanism for decreased renal myostatin expression in uremia.
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