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The Neuroprotective Potential of Cyanidin-3-glucoside Fraction Extracted from Mulberry Following Oxygen-glucose Deprivation
MohammadIqbalHossainBhuiyan, Hyun-BokKim, SeongYunKim, Kyung-OkCho 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.6 6 353-362 (10 pages)
In this study, cyanidin-3-glucoside (C3G) fraction extracted from the mulberry fruit (Morus alba L.) was investigated for its neuroprotective effects against oxygen-glucose deprivation (OGD) and glutamate-induced cell death in rat primary cortical neurons. Cell membrane damage and mitochondrial function were assessed by LDH release and MTT reduction assays, respectively. A time-course study of OGD-induced cell death of primary cortical neurons at 7 days in vitro (DIV) indicated that neuronal... -
The Protective Effect of Quercetin-3-O-β-D-Glucuronopyranoside on Ethanol-induced Damage in Cultured Feline Esophageal Epithelial Cells
JungHyunCho, SunYoungPark, HoSungLee, WanKyunnWhang, UyDongSohn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.6 1 319-326 (8 pages)
Quercetin-3-O-Ղ-D-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus Herba. We aimed to explore its protective effect against ethanol-induced cell damage and the mechanism involved in the effect in feline esophageal epithelial cells (EEC). Cell viability was tested and 2',7'-dichlorofluorescin diacetate assay was used to detect intracellular H2O2 production. Western blotting analysis was performed to investigate MAPK activation and interleukin 6 (IL-6)... -
CD40 Co-stimulation Inhibits Sustained BCR-induced Ca2+ Signaling in Response to Long-term Antigenic Stimulation of Immature B Cells
YenHoangNguyen, Ki-YoungLee, TaeJinKim, SungJoonKim, TongMookKang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.3 9 179-187 (9 pages)
of PLCՃ2 and IP3R-3. Pre-treatment of WEHI-231 cells with the antioxidant N-acetyl-L-cysteine (NAC) strongly inhibited CD40-mediated prevention of the recovery of Ca2+ signaling. In contrast to immature WEHI-231 cells, identical long-term Ձ-IgM pre-stimulation of mature Bal-17 cells abolished the increase in BCR-induced [Ca2+]i, regardless of CD40 co-stimulation. These results suggest that CD40-mediated signaling prevents antigen-induced cell cycle arrest and apoptosis of immature... -
GS28 Protects Neuronal Cell Death Induced by Hydrogen Peroxide under Glutathione-Depleted Condition
HwaOkLee, YuJeongByun, Kyung-OkCho, SeongYunKim, Seong-BeomLee, Ho-ShikKim, Oh-JooKwon, Seong-WhanJeong 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.3 5 149-156 (8 pages)
Golgi SNAP receptor complex 1 (GS28) has been implicated in vesicular transport between intra-Golgi networks and between endoplasmic reticulum (ER) and Golgi. Additional role(s) of GS28 within cells have not been well characterized. We observed decreased expression of GS28 in rat ischemic hippocampus. In this study, we examined the role of GS28 and its molecular mechanisms in neuronal (SK-N-SH) cell death induced by hydrogen peroxide (H2O2). GS28 siRNA-transfected cells treated with H2O2 showed... -
HO-1 Induced by Cilostazol Protects Against TNF-α-associated Cytotoxicity via a PPAR-γ-dependent Pathway in Human Endothelial Cells
SoYounPark, JinUngBae, KiWhanHong, ChiDaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.2 2 83-88 (6 pages)
of the antioxidant enzyme heme oxygenase-1 (HO-1) in synovial cells. Thus, the present study was undertaken to examine whether cilostazol is able to counteract tumor necrosis factor-Ձ (TNF-Ձ)-induced cell death in endothelial cells via the induction of HO-1 expression. We exposed human umbilical vein endothelial cells (HUVECs) to TNF-Ձ (50 ng/ml), with or without cilostazol (10ՌM). Pretreatment with cilostazol markedly reduced TNF-Ձ-induced viability loss in the... -
Involvement of ROS in Curcumin-induced Autophagic Cell Death
YounJuLee, Nam-YiKim, Young-AhSuh, ChuHeeLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.1 1 1-8 (8 pages)
It was further confirmed that treatment of cells with hydrogen peroxide induced increase of LC3 conversion and decrease of GFP-LC3 and SQSTM1 levels, but these changes by curcumin were almost completely blocked in the presence of antioxidant, N-acetylcystein (NAC), indicating that curcumin leads to reactive oxygen species (ROS) production, which results in autophagosome development and autolysosomal degradation. In parallel with NAC, SQSTM1 degradation was also diminished by bafilomycin A, a... -
Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice
Hye-NaCha, JungHyunChoi, Yong-WoonKim, Jong-YeonKim, Myun-WhanAhn, So-YoungPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.6 5 377-384 (8 pages)
collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress. -
Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells
HeeYulAhn, ChanHyungKim, Tae-SunHa 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 12 325-329 (5 pages)
Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might... -
Bark Constituents from Mushroom-detoxified Rhus verniciflua Suppress Kainic Acid-induced Neuronal Cell Death in Mouse Hippocampus
Jong-SeonByun, YoonHeeHan, Sung-JunHong, Sung-MiHwang, Yong-SooKwon, HeeJaeLee, Sung-SooKim, Myong-JoKim, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 5 279-283 (5 pages)
as anti-inflammatory, antioxidant, and anti-cancer actions. To reduce the urushinol content while maintaining the beneficial biological activities, mushroom-mediated fermentation of Rhus verniciflua was carried out and this method resulted in significantly attenuated allergenicity [1]. In the present study, to examine the neuroprotective properties of mushroom-fermented stem bark of Rhus verniciflua, two constituents were isolated from mushroom-fermented bark and their neuroprotective properties... -
Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells
DaeGoonYoo, CukSeongKim, SangKiLee, HyoShinKim, EunJungCho, MyoungSooPark, SangDoLee, JinBongPark, ByeongHwaJeon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.3 4 139-144 (6 pages)
In this study, we evaluated the role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the tumor necrosis factor-Ձ (TNF-Ձ) induced cyclooxygenase-2 (COX-2) expression using A549 lung adenocarcinoma cells. TNF-Ձ induced the expression of COX-2 in A549 cells, but did not induce BEAS-2B expression. The expression of COX-2 in A549 cells was TNF-Ձ dose-dependent (5∼100 ng/ml). TNF-Ձ-stimulated A549 cells evidenced increased Ref-1 expression in a...


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