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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Biomed+Res+Int 2015 ; 2015 (ä): ä Nephropedia Template TP
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Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain #MMPMID26448932
Kim CK; Yang XL; Kim YJ; Choi IY; Jeong HG; Park HK; Kim D; Kim TJ; Jang H; Ko SB; Yoon BW
Biomed Res Int 2015[]; 2015 (ä): ä PMID26448932show ga
Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5?mg/kg) or regular doses (1 or 3?mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5?mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41?mm3 for 0.5?mg/kg and 153 ± 47?mm3 for PBS-control with MCAO; P < 0.01) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of I?B and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.