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류혜명,최순윤,김용림 계명대학교 자연과학연구소 2015 Quantitative Bio-Science Vol.34 No.1
Recombinant human erythropoietin (EPO), a glycohormone, is one of the leading biopharmaceutical products, while carbamylated erythropoietin (CEPO), an EPO derivative, is attracting widespread interest due to its neuroprotective effects without erythropoiesis in several cells and animal models. However, the protective effects of CEPO on renal fibrosis still remain unknown. In this study, we evaluated the inhibitory effects of CEPO against transforming growth factor (TGF)-β1-induced epithelial-to-mesenchymal transition (EMT) in Madin-Darby Canine Kidney (MDCK) cells. MDCK cells were treated with TGF-β1 (5 ng/mL) for 48 h to induce EMT, and the cells were then co-treated with TGF-β1 and CEPO or recombinant human EPO for another 48 h. Increased expressions of α-smooth muscle actin (α-SMA) and decreased expressions of E-cadherin were observed after TGF-β1 treatment, and these changes were markedly attenuated by CEPO co-treatment. TGF-β1 increased phosphorylated Smad-2 expression in MDCK cells, which was decreased by CEPO cotreatment. The results indicate that CEPO ameliorates the TGF-β1-induced EMT mediated by p-Smad2 pathway. It suggests that CEPO has therapeutic potential in chronic kidney disease.
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Fimasartan attenuates renal ischemia-reperfusion injury by modulating inflammation-related apoptosis
조장희,최순윤,류혜명,오은주,육주민,안지선,정희연,최지영,박선희,김찬덕,김용림 대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.6
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.
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