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Monoamine Oxidase Inhibitors Attenuate Cytotoxicity of 1-Methyl-4-phenylpyridinium by Suppressing Mitochondrial Permeability Transition
ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 7 207-212 (6 pages)
Mitochondrial permeability transition has been shown to be involved in neuronal cell death. Mitochondrial monoamine oxidase (MAO)-B is considered to play a part in the progress of nigrostriatal cell death. The present study examined the effect of MAO inhibitors against the toxicity of 1-methyl-4- phenylpyridinium (MPP) in relation to the mitochondrial permeability transition. Chlorgyline (a selective inhibitor of MAO-A), deprenyl (a selective inhibitor of MAO-B) and tranylcypromine (non-... -
Effect of Rosiglitazone on Myocardial Ischemia-Reperfusion Injury in Rat Heart
Ki-ChanHa 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 3 181-186 (6 pages)
This study was undertaken to evaluate whether peroxisome proliferator-activated-receptor-gamma (PPAR-γ) agonist-rosiglitazone (ROSI) induces postischemic functional recovery in Langendorf heart model. Hearts isolated from normal rats were subjected to 20 min of normoxia or 25 min zero-flow ischemia followed by 50 min reperfusion. In this acute protocol, ROSI (20μg/ml) administered 10 min before ischemia had no effect on hemodynamic cardiac function, but had protective effect on lipid... -
Gene Expression Profile in Microglia following Ischemia- Reperfusion Injury
JuHyeonOh, HyungSooHan, JaeSikPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 2 173-180 (8 pages)
Microglial activation is thought to play a role in the pathogenesis of many brain disorders. Therefore, understanding the response of microglia to noxious stimuli may provide insights into their role in disorders such as stroke and neurodegeneration. Many genes involved in this response have been identified individually, but not systematically. In this regards, the microarray system permitted to screen a large number of genes in biological or pathological processes. Therefore, we used microarray... -
Nitric Oxide Donor, NOR-3, Increased Expression of Cyclooxygenase-2, but not of Cyclooxygenase-1 in Cultured VSMC
DongHyupLee, JiEunPark, YoungJinKang, KwangYounLee, HyoungChulChoi 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.3 8 161-165 (5 pages)
the effects of NO donors on the COX-1 and COX-2 mRNA/protein expression, as well as the nitrite production in culture medium of vascular smooth muscle cell (VSMC). VSMC was primarily cultured from thoracic aorta of rat. In this experiments, COX-1 and COX-2 mRNA/protein expressions were analysed and nitrite productions were investigated using Griess reagent. VSMC did not express COX-2 protein in basal condition (Non- lipopolysaccharide (LPS) stimulated). In LPS-stimulated experiments, after 3... -
Protective Effect of Defibrotide on Splanchnic Injury following Ischemia and Reperfusion in Rats
SooRanChoi, JiHoonJeong, JinHoSong, YongKyooShin 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.2 5 85-94 (10 pages)
to superior mesentric artery segments. Superoxide anion and hydrogen peroxide production in 1μM formylmethionylleucylphenylalanine (fMLP)-activated PMNs was inhibited by defibrotide in a dose-dependent fashion. Defibrotide effectively scavenged hydrogen peroxide, but not hydroxyl radical. Treatment of SAO rats with defibrotide inhibited tumor necrosis factor-α, and interleukin-1β productions in blood in comparison with untreated rats. These results suggest that defibrotide partly provides... -
Promoting Effect of Hydrogen Peroxide on 1-Methyl-4-phenylpyridinium-induced Mitochondrial Dysfunction and Cell Death in PC12 Cells
DongHeeLee, ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.1 9 51-57 (7 pages)
The promoting effect of hydrogen peroxide (H2O2) against the cytotoxicity of 1-methyl-4-phenylpyridinium (MPP) in differentiated PC12 cells was assessed by measuring the effect on the mitochondrial membrane permeability. Treatment of PC12 cells with MPP resulted in the nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species (ROS) and depletion of GSH.... -
Differential Activation of Ras/Raf/MAPK Pathway between Heart and Cerebral Artery in Isoproterenol-induced Cardiac Hypertrophy
HyunjuKim, NariKim, HyunJoo, JaeBoumYoum, WonSunPark, MohamedWarda, SunghyunKang, VuThiThu, TranMinhKhoa, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.5 7 299-304 (6 pages)
Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO)-evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery,... -
Differential Inhibition of MPP+- or 6-Hydroxydopamine-induced Cell Viability Loss in PC12 Cells by Trifluoperazine and W-7
ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 9 247-252 (6 pages)
c and caspase-3 activation in PC12 cells treated with MPP and attenuated the formation of reactive oxygen species and the depletion of GSH, whereas both compounds did not reduce the effect of 6-OHDA. The results show that trifluoperazine and W-7 may attenuate the cytotoxicity of MPP by inhibition of the mitochondrial permeability transition and calmodulin. Meanwhile, the cytotoxic effect of 6-OHDA seems to be mediated by the actions, which are different from MPP..pdf -
Inhibition of Nitric Oxide-induced Neuronal Apoptosis in PC12 Cells by Epigallocatechin Gallate
JiYeonJung, YeonJinJeong, ChangRyoungHan, SunHunKim, HyunJinKim, KiHeonLee, HaOkPark, WonJaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 8 239-246 (8 pages)
fragmentation with cell shrinkage and chromatin condensation. EGCG diminished the decrement of cell viability and the formation of apoptotic morphologenic changes as well as DNA fragmentation by SNP. EGCG played as an antioxidant that attenuated the production of reactive oxygen species (ROS) by SNP. The cells treated with SNP showed downregulation of Bcl-2, but upregulation of Bax. EGCG ameliorated the altered expression of Bcl-2 and Bax by SNP. The release of cytochrome c from mitochondria int... -
Inhibition of Hypoxia-induced Apoptosis in PC12 Cells by Estradiol
JiYeonJung, KwangHoonRoh, YeonJinJeong, SunHunKim, EunJuLee, MinSeokKim, WonMannOh, HeeKyunOh, WonJaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 7 231-238 (8 pages)
increase in the release of cytochrome c from mitochondria into cytoplasm and Fas-ligand (Fas-L) upregulated by CoCl2. These results suggest that CoCl2 induce apoptosis in PC12 cells through both mitochondria- and death receptor-mediated cell death pathway. Estradiol was found to have a neuroprotective effect against CoCl2-induced apoptosis through the inhibition of ROS production and by modulating apoptotic effectors associated with the mitochondria- and death-dependent pathway in PC12 cells.


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