Hye Young Son

Dongguk University, Sŏul, Seoul, South Korea

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Publications (4)8.97 Total impact

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    ABSTRACT: Endothelial dysfunction is involved in stroke. Recent therapeutic options for stroke have focused on the combination therapy with a polyherbal mixture. This study was designed to provide insight into the effects of JP05, a water extract of 12 herbs, on the levels of regulators in bEnd.3 mouse brain endothelial cells. Production of endothelial nitric oxide synthase (eNOS)-mediated nitric oxide (NO), the expression of vascular endothelial growth factor (VEGF) and the phosphorylations of eNOS, phosphatidylinositol 3-kinase (PI3K)/Akt, extracellular signal-regulated protein kinase (ERK) and cAMP response element binding protein (CREB) in JP05 were assayed in bEnd.3 cells, a mouse brain endothelial line. JP05 led to increase the levels of eNOS-mediated NO generation and VEGF expression in bEnd.3 cells. JP05 induced the phosphorylation of eNOS, Akt and ERK in bEnd.3 cells. As well, JP05 blocked the inhibition of PI3K/Akt and ERK activities by LY294002 (PI3K/Akt inhibitor) and PD98059 (mitogen-activated protein kinase inhibitor), respectively. JP05 also induced the phosphorylation of CREB, which plays an important role in endothelial cell function and blood vessel development. Taken together, these results indicate that JP05 can upregulate eNOS-mediated NO generation and VEGF expression through the ERK and/or PI3K/Akt activation, an upstream event of angiogenesis. JP05 with vasoprotective properties has a potential therapy for human brain diseases including stroke.
    Journal of ethnopharmacology 08/2010; 130(3):607-13. DOI:10.1016/j.jep.2010.05.050 · 2.32 Impact Factor
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    ABSTRACT: Many current studies of Parkinson's disease (PD) suggest that inflammation is involved in the neurodegenerative process. PD-1, a traditional Korean medicine, used to treat various brain diseases in Korea. This study was designed to investigate the effect of PD-1 extract in the Parkinson's model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned mice. The MPTP administration caused the dopamine neuron loss in the striatum and substantia nigra pars compacta (SNpc), which was demonstrated by a depletion of tyrosine hydroxylase (TH). In addition, a reduction of bcl-2 expression with elevation of bax expression, caspase-3 activation, and release of cytochrome c into cytosol in dopaminergic neurons of SNpc were noted. Oral administration of PD-1 extract (50 and 100 mg kg(-1)) attenuated the MPTP-induced depletion of TH proteins in the striatum and SNpc and prevented the apoptotic effects. These results indicate that PD-1 extract is able to protect dopaminergic neurons from MPTP-induced neuronal death, with important implications for the treatment of PD.
    Cell Biochemistry and Function 02/2010; 28(3):217-23. DOI:10.1002/cbf.1642 · 2.13 Impact Factor
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    ABSTRACT: The roots of Panax notoginseng (PN) are commonly used as a therapeutic agent to stop hemorrhage and as a tonic to promote health in traditional Korean medicine. Stroke triggers an inflammatory response that not only plays a central role in the pathogenesis of cerebral ischemia, but also induces secondary damage. This study was designed to investigate the neuroprotective effects of the methanol extract of PN on the infarct volume induced by middle cerebral artery occlusion (MCAO) (90-min occlusion and 24-h reperfusion) in rat brains. The PN extract (50 mg/kg, i.p.) was administered 2 h after the onset of MCAO. The PN-treated groups had a reduction in infarct volume by 23.82 +/- 8.9%. In the PN extract-treated groups, the microglial density was significantly decreased in the peri-infarct region; the underlying mechanism was inhibition of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, via blocking of the NF-kappaB pathway. Furthermore, in vitro studies showed that the PN extract significantly reduced the production of iNOS-derived NO and COX-2-derived prostaglandin E(2) through the regulation of gene transcription levels in primary microglia and BV-2 cells. These results suggest that anti-inflammatory and microglial activation inhibitory effects of the PN extract may contribute to its neuroprotective effects in brain ischemia.
    Journal of Pharmacological Sciences 04/2009; 109(3):368-79. DOI:10.1254/jphs.08197FP · 2.11 Impact Factor
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    ABSTRACT: Excessive production of inflammatory mediators, nitric oxide (NO) and proinflammatory cytokines from activated microglia has been implicated in neurodegeneration in human brain diseases. Recently, it seems possible that treatment with antiinflammatory agents, including Oriental medicinal plants, might delay the progression of neurodegeneration through the inhibition of microglial activation. The present study evaluated the effect of a methanol extract of Ficus religiosa leaf (MFL) on lipopolysaccharide (LPS)-induced production of NO and proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-beta (IL-1beta) and IL-6 in BV-2 cells, a mouse microglial line. MFL inhibited LPS-induced production of NO and proinflammatory cytokines in a dose-dependent manner. MFL also attenuated the expression of mRNA and proteins of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines, suggesting the blockage of transcription levels, respectively. The molecular mechanism of MFL-mediated attenuation underlies the down-regulation of the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signaling pathway, and suppresses the nuclear factor kappaB (NF-kappaB) activation. The results suggest that MFL exhibits antiinflammatory properties in LPS-induced activation of BV2 microglial cells, and that might have a therapeutic potential for various neurodegenerative diseases.
    Phytotherapy Research 06/2008; 22(8):1064-9. DOI:10.1002/ptr.2442 · 2.40 Impact Factor