학술논문
Fimasartan attenuates renal ischemia-reperfusion injury by modulating inflammation-related apoptosis
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- 영문명
- Fimasartan attenuates renal ischemia-reperfusion injury by modulating inflammation-related apoptosis
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Jang-Hee Cho Soon-Youn Choi Hye-Myung Ryu Eun-Joo Oh Ju-Min Yook Ji-Sun Ahn Hee-Yeon Jung Ji-Young C
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제22권 제6호, 661~670쪽, 전체 10쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2018.11.30
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국문 초록
영문 초록
Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor (TNF)-α, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of TNF-α, interleukin (IL)-1β, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
CONFLICTS OF INTEREST
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