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Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways
YanjiCui, Jee-YunPark, JinjiWu, JiHyungLee, Yoon-SilYang, Moon-SeokKang, Sung-CherlJung, JooMinPark, Eun-SookYoo, Seong-HoKim, SangmeeAhnJ 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.3 5 219-228 (10 pages)
attenuated Akt phosphorylation and increased expression of gp91phox, which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein... -
Cyanidin-3-glucoside Inhibits ATP-induced Intracellular Free Ca2+ Concentration, ROS Formation and Mitochondrial Depolarization in PC12 Cells
ShaziaPerveen, JiSeonYang, TaeJoungHa, ShinHeeYoon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.4 3 297-305 (9 pages)
the formation of ROS in the presence of cyanidin-3-glucoside. All these results suggest that cyanidin-3-glucoside inhibits ATP-induced calcium signaling in PC12 cells by inhibiting multiple pathways which are the influx of extracellular Ca2+ through the nimodipine and ω-conotoxin-sensitive and -insensitive pathways and the release of Ca2+ from intracellular stores. In addition, cyanidin-3-glucoside inhibits ATP-induced formation of ROS by inhibiting Ca2+-induced mitochondrial depolarization. -
Bcl-2 Knockdown Accelerates T Cell Receptor-Triggered Activation-Induced Cell Death in Jurkat T Cells
Yun-JungLee, TaeJoonWon, KyeongEunHyung, MiJiLee, Young-hyeMoon, IkHeeLee, ByungSungGo, KwangWooHwang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.1 10 73-78 (6 pages)
Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2... -
(-)-Epigallocatechin-3-gallate Modulates the Differential Expression of Survivin Splice Variants and Protects Spermatogenesis During Testicular Torsion
NadaAl-Ajmi, MayAl-Maghrebi, WaleedMohammedRenno 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.4 2 259-265 (7 pages)
of apoptosis induction. Histological analyses revealed increased DNA fragmentation and increased damage to spermatogenesis associated with decreased seminiferous tubular diameter and decreased germinal epithelial cell thickness in the TT/D+vehicle group. These changes were reversed to almost sham levels upon EGCG treatment. Our data indicate that EGCG protects the testis from TT/D-induced damage by protecting the morphology of the seminiferous tubules and modulating survivin 140 expression. -
2-(4-Hydroxyphenyl)-5-(3-Hydroxypropenyl)-7-Methoxybenzofuran, a Novel Ailanthoidol Derivative, Exerts Anti-Inflammatory Effect through Downregulation of Mitogen-Activated Protein Kinase in Lipopolysaccharide-Treated RAW 264.7 Cells
HyeonJinKim, Jong-GabJun, Jin-KyungKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.3 6 217-222 (6 pages)
(compounds 1-6). Among them, compound 4, 2-(4-hydroxyphenyl)-5-(3-hydroxypropenyl)-7-methoxybenzofuran, had the lowest IC50 value concerning nitric oxide (NO) release from lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Compound 4 suppressed the generation of prostaglandin (PG) E2 and the expression of inducible NO synthase and cyclooxygenase (COX)-2 induced by LPS, and inhibited the release of LPS-induced pro-inflammatory cytokines from RAW264.7 cells. The underlying mechanism of compound 4... -
5,8-Dimethoxy-2-Nonylamino-Naphthalene-1,4-DioneInhibitsVascular Smooth Muscle Cell Proliferation by Blocking Autophosphorylation of PDGF-Receptor β
YohanKim, Jung-JinLee, Sang-GilLee, Sang-HyukJung, Joo-HuiHan, SoYoungYang, , EunjuYun, Gyu-YongSong, Chang-SeonMyung 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.3 4 203-208 (6 pages)
synthesized naphthoquinone derivative, 5,8-dimethoxy-2-nonylamino-naphthalene-1,4-dione (2-nonylamino- DMNQ), using VSMCs treated with platelet-derived growth factor (PDGF). 2-Nonylamino-DMNQ inhibited proliferation and cell number of VSMCs induced by PDGF, but not epidermal growth factor (EGF), in a concentration-dependent manner without any cytotoxicity. This derivative suppressed PDGF-induced [3H]-thymidine incorporation, cell cycle progression from G0/G1 to S phase, and the phosphorylation... -
Insulin Like Growth Factor Binding Protein-5 Regulates Excessive Vascular Smooth Muscle Cell Proliferation in Spontaneously Hypertensive Rats via ERK 1/2 Phosphorylation
DongHyupLee, JungEunKim, YoungJinKang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.2 7 157-162 (6 pages)
in the VSMCs of WKY as much as those of SHR. Concurrent treatment with the MEK1/2 inhibitors, PD98059 or U0126 completely inhibited recombinant IGFBP-5-induced VSMC proliferation in WKY, while concurrent treatment with the phosphatidylinositol-3 kinase inhibitor, LY294002, had no effect. Furthermore, knockdown with IGFBP-5 siRNA inhibited ERK1/2 phosphorylation in VSMC of SHR. These results suggest that IGFBP-5 plays a role in the regulation of VSMC proliferation via ERK1/2 MAPK signaling in... -
Ginsenoside Rg2 Inhibits Lipopolysaccharide-Induced Adhesion Molecule Expression in Human Umbilical Vein Endothelial Cell
Young-SukCho, ChanHyungKim, Tae-SunHa, SangJinLee, HeeYulAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.2 4 133-137 (5 pages)
in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-ՊB) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1... -
Differential Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on Motor Behavior and Dopamine Levels at Brain Regions in Three Different Mouse Strains
Keun-SungLee, Jin-KooLee, Hyung-GunKim, HakRimKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2013, Vol.17 No.1 13 89-97 (9 pages)
mechanism of the disease and allows testing of newly developed new drugs before human application. However, which of the plethora of experimental animal species to use in model development can be perplexing. Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a very well known method to induce the symptoms of Parkinson's disease in mice. But, there is very limited information about the different sensitivities to MPTP among mouse strains. Here, we tested three different mouse... -
Induction of Heat Shock Proteins and Antioxidant Enzymes in 2,3,7,8-TCDD-Induced Hepatotoxicity in Rats
Hyun-SookKim, So-YoungPark, Ki-YeolYoo, SeungKwanLee, Woon-WonJung 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2012, Vol.16 No.6 14 469-476 (8 pages)
shock protein (Ձ-B-crystallin, Hsp90, and GRP78) and antioxidant enzymes (SOD-1, SOD-3, catalase, GST, and GPXs) expression decreased on day 2 and then slowly recovered back to control levels on day 8. These results suggest that heat shock proteins and antioxidant enzymes were induced as protective mechanisms against 2,3,7,8-TCDD induced hepatotoxicity, and that prolonged exposure depressed their levels, which recovered to control levels due to reduced 2,3,7,8-TCDD induced hepatotoxicity.


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