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RISS 인기검색어
- 검색키워드
- 저자 : Eda Aypar (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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The Mechanism of the Late Preconditioning Effect of 3-Nitropropionic Acid
Basgut, Bilgen,Aypar, Eda,Basgut, Ertug,Akin, K. Okhan,Kilic, Nedret,Cakici, Idal 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.10
The aim of the present study was to investigate the mechanism of effect of 3-nitropropionic acid- (3-NP) induced late preconditioning in rat heart. For this purpose 20-30 min before 3-NP (20 mg/kg, i.p.) injection, the rats were treated intraperitoneally with 5-hydroxydecanoate (40 mg/kg, 5-HD, mitochondrial $K_{ATP}$-channel blocker), L-NAME (100 mg/kg, NOS inhibitor), N-2-mercaptopropionylglycine (100 mg/kg, MPG, free radical scavenger), or superoxide dismutase+catalase (10000+10000 IU/kg, SOD+CAT). Control rats received saline only without 3-NP pretreatment. After two days, hearts were isolated and perfused at a constant pressure in a Langendorff apparatus. 15-min global ischemia followed by 30-min reperfusion was applied to all hearts. Pretreatment of 3-NP significantly reduced infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) levels, and incidence of ventricular tachycardia (VT) compared with the control group receiving saline only. 5-HD, L-NAME, MPG, or SOD+CAT treatment statistically reversed 3-NP-induced reduction in infarct size. Although CK-MB, LDH levels, and incidence of VT were also reduced by L-NAME, MPG, or SOD+CAT treatment, only 5-HD significantly inhibited beneficial effects of 3-NP on all of the parameters above. These results showed that mito-$K_{ATP}$ channels play a pivotal role in late preconditioning effect of 3-NP in the isolated rat heart. However, other mediators such as reactive oxygen species and NO may be, at least in part, involved in mechanisms of this effect.
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The Mechanism of the Late Preconditioning Effect of 3-Nitropropionic Acid
Bilgen Basgut,Eda Aypar,Ertug Basgut,K. Okhan Akln,Nedret Klllc,And Iclal Caklcl 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.10
The aim of the present study was to investigate the mechanism of effect of 3-nitropropionic acid- (3-NP) induced late preconditioning in rat heart. For this purpose 20-30 min before 3-NP (20 mg/kg, i.p.) injection, the rats were treated intraperitoneally with 5-hydroxydecanoate (40 mg/kg, 5-HD, mitochondrial KATP-channel blocker), L-NAME (100 mg/kg, NOS inhibitor), N-2-mercaptopropionylglycine (100 mg/ kg , MPG, free radical scavenger), or superoxide dismutase+catalase (10000+10000 IU/kg , SOD+CAT). Control rats received saline only without 3-NP pretreatment. After two days, hearts were isolated and perfused at a constant pressure in a Langendorff apparatus. 15- min global ischemia followed by 30-min reperfusion was applied to all hearts. Pretreatment of 3-NP significantly reduced infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) levels, and incidence of ventricular tachycardia (VT) compared with the control group receiving saline only. 5-HD, L-NAME, MPG, or SOD+CAT treatment statistically reversed 3-NP-induced reduction in infarct size. Although CK-MB, LDH levels, and incidence of VT were also reduced by L-NAME, MPG, or SOD+CAT treatment, only 5-HD significantly inhibited beneficial effects of 3-NP on all of the parameters above. These results showed that mito-KATP channels play a pivotal role in late preconditioning effect of 3-NP in the isolated rat heart. However, other mediators such as reactive oxygen species and NO may be, at least in part, involved in mechanisms of this effect.
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Chronic ouabain treatment induces Rho kinase activation
Aysun Ozdemir,Gürkan Şahan,Ayşegül Demirtas,Eda Aypar,Gürkan Gözübüyük,Nilüfer Nermin Turan,Mustafa Ark 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.10
Ouabain is an endogenous Na?/K?-ATPaseinhibitor whose chronic administration induces hypertension. Endogenous ouabain levels increase in humanessential hypertension. On the other hand, Rho/Rho kinase(ROCK) pathway has been implicated in various animalmodels of hypertension. In the current work, we evaluatedthe possible involvement of Rho kinase in ouabain-inducedhypertension. Ouabain was administered daily (20 lg/kg,i.p.) to Wistar rats for 6 weeks. After the ouabain treatment,we evaluated the possible changes in vascular responsesto KCl and phenylephrine alone and in thepresence of Rho kinase inhibitor Y27632. We also determinedthe expressions of ROCKs, Rho A and phosphorylationof myosin binding subunit of myosin light chainphosphatase (pMYPT) and activation of Rho A. Agonistinducedcontractions in the presence of Y27632 are significantlydecreased and Y27632-induced relaxations inaortas precontracted with phenylephrine are significantlyenhanced with the chronic treatment of ouabain. Althoughthe expressions of ROCK I and ROCK II remained unchanged,pMYPT expression was significantly increased inouabain-treated group. Moreover, Rho A expression andactivation were decreased after treatment with ouabain. Although Rho kinase expression did not change in aortas,increased basal Rho kinase activation may contribute to thedevelopment of ouabain-induced hypertension. Our currentdata present the first evidence that Rho kinase is involvedin the development of ouabain-induced hypertension inrats.
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