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RISS 인기검색어
- 검색키워드
- 저자 : Sadayoshi Ito (검색결과 4 건)
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안경옥,임선우,양현주,Can Li,Akira Sugawara,Sadayoshi Ito,최범순,김용수,김진,양철우 연세대학교의과대학 2007 Yonsei medical journal Vol.48 No.2
Purpose: We recently reported that rosiglitazone (RGTZ), a peroxisome proliferator-activated receptor gamma (PPARγ) agonist, has a protective effect against cyclosporine (CsA)- induced renal injury. Here we report the effect of RGTZ on peroxisome proliferator-activated receptor gamma (PPARγ) expression in an experimental model of chronic cyclosporine (CsA) nephropathy. Materials and Methods: Chronic CsA nephropathy was induced in Sprague-Dawley rats by administering CsA (15mg/kg per day) for 28 days, and control rats were treated with vehicle (VH group, olive oil 1mL/kg per day) for 28 days. RGTZ (3mg/kg) was concurrently administered via gavage to the CsA and VH groups. Expression of PPARγ mRNA and protein was evaluated with RT-PCR, immunohistochemistry, and immunoblotting. Results: PPARγ mRNA expression was similar to the level of PPARγ protein constitutively expressed in the kidneys of the VH treated rats, with expression in the glomerular epithelial, distal tubular cells, and collecting tubular cells. PPARγ protein expression in CsA-treated rat kidneys was significantly less than in the VH group. However, concomitant administration of RGTZ restored PPARγ protein expression in the kidneys of the CsA- reated rats. Conclusion: Exogenous administration of RGTZ treatment upregulates PPARγ expression and that this mechanism may play a role in protecting against CsA-induced renal injury.
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CHUNG, BYUNG HA,LIM, SUN WOO,AHN, KYUNG OHK,SUGAWARA, AKIRA,ITO, SADAYOSHI,CHOI, BUM SOON,KIM, YONG SOO,BANG, BYUNG KEE,YANG, CHUL WOO Blackwell Science Pty 2005 Nephrology Vol.10 No.suppl2
<P>SUMMARY: </P><P>Peroxisome proliferator activated receptor gamma (PPAR&ggr;) agonist has not only antidiabetic effect but also a protective effect against various types of injury of the kidney. The protective effects of PPAR&ggr; agonists are observed in diabetic nephropathy and non-diabetic renal diseases such as 5/6 ablation model of renal failure, experimental glomerulonephritis, ischemia-reperfusion injury, hypertensive nephropathy and cyclosporin-induced renal injury. The mechanism of renoprotection by PPAR&ggr; agonist is multifactorial. Anti-fibrotic and anti-inflammatory effects, suppression of renin-angiotensin system, vascular protective effect and antiapoptotic effect were proposed.</P>
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Review : PPARγ Agonist Beyond Glucose Lowering Effect
( Akira Sugawara ),( Akira Uruno ),( Masataka Kudo ),( Ken Matsuda ),( Chul Woo Yang ),( Sadayoshi Ito ) 대한내과학회 2011 The Korean Journal of Internal Medicine Vol.26 No.1
The nuclear hormone receptor PPARγ is activated by several agonists, including members of the thiazolidinedione group of insulin sensitizers. Pleiotropic beneficial effects of these agonists, independent of their blood glucose- lowering effects, have recently been demonstrated in the vasculature. PPARγ agonists have been shown to lower blood pressure in animals and humans, perhaps by suppressing the renin-angiotensin (Ang)-aldosterone system (RAAS), including the inhibition of Ang II type 1 receptor expression, Ang-II-mediated signaling pathways, and Ang-II-induced adrenal aldosterone synthesis/secretion. PPARγ agonists also inhibit the progression of atherosclerosis in animals and humans, possibly through a pathway involving the suppression of RAAS and the thromboxane A2 system, as well as the protection of endothelial function. Moreover, PPARγ-agonist-mediated renal protection, especially the reduction of albuminuria, has been observed in diabetic nephropathy, including animal models of the disease, and in non-diabetic renal dysfunction. The renal protective activities may reflect, at least in part, the ability of PPARγ agonists to lower blood pressure, protect endothelial function, and cause vasodilation of the glomerular efferent arterioles. Additionally, anti-neoplastic effects of PPARγ agonists have recently been described. Based on the multiple therapeutic actions of PPARγ agonists, they will no doubt lead to novel approaches in the treatment of lifestyle-related and other diseases. (Korean J Intern Med 2011;26:19-24)
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Rosiglitazone Protects Against Cyclosporine-Induced Pancreatic and Renal Injury in Rats
Chung, Byung Ha,Li, Can,Sun, Bo Kyung,Lim, Sun Woo,Ahn, Kyung Ohk,Yang, Ji Hun,Choi, Yoon Hee,Yoon, Kun Ho,Sugawara, Akira,Ito, Sadayoshi,Kim, Jin,Yang, Chul Woo Wiley (Blackwell Publishing) 2005 American journal of transplantation Vol.5 No.8
<P>Rosiglitazone (RGTZ) has protective effect against various types of injury. This study was performed to evaluate the effect of RGTZ on pancreatic and renal injury caused by cyclosporine (CsA). CsA (15 mg/kg) and RGTZ (3 mg/kg) were administered alone and together to the rats for 28 days. The effect of RGTZ on CsA-induced pancreatic injury was evaluated by intraperitoneal glucose tolerance test (IPGTT), plasma insulin concentrations and pancreatic beta-cell morphology. The effect of RGTZ on CsA-induced renal injury was evaluated by assessing renal function and pathology; mediators of inflammation and fibrosis such as angiotensin II (AngII), osteopontin (OPN) and transforming growth factor-beta1 (TGF-beta1) and apoptotic cell death. Four weeks of CsA treatment caused diabetes, renal dysfunction, typical pathologic lesions (arteriolopathy, interstitial fibrosis and inflammatory cells infiltration) and apoptotic cell death. RGTZ treatment decreased blood glucose concentration, increased plasma insulin concentration and preserved pancreatic beta islet mass. RGTZ treatment improved renal function and histopathology. Pro-inflammatory and pro-fibrotic molecules such as AngII, OPN and TGF-beta1, and apoptotic cell death also decreased with RGTZ treatment. These data suggest that RGTZ has a protective effect against CsA-induced pancreatic and renal injury.</P>
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