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논문분류	춘계학술대회 초록집
제목	The PPAR-α Agonist Fenofibrate Ameliorates Aging-related Progressive Renal Injury
저자	Eun Nim Kim1, Ji Hee Lim1, Min Young Kim1, Byung Ha Chung1, Cheol Whee Park1,Chul Woo Yang1, Yong-Soo Kim1, Yoon Sik Chang2, Bum Soon Choi1
출판정보	2014; 2014(1):
키워드	노화, 신장, PPAR-α, SIRT1
초록	Background: Aging is a multifactorial process characterized by a progressive decline in physiological function. Peroxisome proliferator-activated receptor-α (PPAR-α) is key regulators in various age-associated physiological processes related to energy metabolism and oxidative stress. We therefore examined the activation of PPAR-α by PPARa agonists fenofibrate would improve changes of aging and oxidative stress in the kidney. Methods: Male 19-month-old C57/BL6 mice were used in this study. Fenofibrate (0.1%) was provided to old mice for 6 month. We measured histological change, oxidative stress, and aging-related protein expression in the kidneys. Results: Fenofibrate-treated old-mice displayed decreased albuminuria (59.4±31 ng/24hr vs. 22.7±8.5 ng/24hr; p<0.05 vs. VH). Creatinine clearance increased with Fenofibrate-treated old-mice (0.07±0.04 ml/min vs. 0.16±0.05 ml/min; p<0.05 vs. VH). Serum creatinine was decreased in Fenofibrate-treated old-mice, although this was not statistically significant (0.75±0.3 mg/dL vs. 0.44±0.2 mg/dL). There were decreases in mesangial volume (56.1±2.06% vs. 42.87± 1.25%; p<0.001 vs. VH) and tubulointerstitial fibrosis (16.1±4.32% vs. 4.41±3.61%; p<0.001 vs. VH) in Fenofibrate- treated old-mice. In our study, expression of PPARa (1±0.2 fold vs. 1.31±0.11 fold; p<0.05 vs. VH) was increased in Fenofibrate-treated old-mice. SIRT1 expression (1±0.2 fold vs. 1.97±0.23 fold; p<0.05 vs. VH) was increased in Fenofibrate-treated old-mice compared with control-old mice. Also, expression of PGC-1a (1±0.07 fold vs. 1.85±0.13 fold; p<0.05 vs. VH) was increased in Fenofibrate-treated old-mice. Conclusions: These results suggest that PPAR-α agonists may benefit aging-related renal injury by SIRT1 activation. Pharmacologically targeting PPAR-α and SIRT1 signaling molecules may reduce the pathologic changes of aging in the kidney.
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