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Sokho Kim,Myung-Hoon Oh,Bum-Seok Kim,Won-Il Kim,Ho-Seong Cho,Byoung-Yong Park,Chul Park,Gee-Wook Shin,Jungkee Kwon 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.4
Background: The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been suffi- ciently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GRo in vitro using the Raw 264.7 mouse macrophage cell line treated with lipopolysaccharide (LPS), and to clarify the possible mechanism of GRo involving heme oxygenase-1 (HO-1), which itself plays a critical role in self-defense in the presence of inflammatory stress. Methods: Raw 264.7 cells were pretreated with GRo (up to 200mM) for 1 h before treatment with 1 mg/ mL LPS, and both cell viability and inflammatory markers involving HO-1 were evaluated. Results: GRo significantly increased cell viability in a dose dependent manner following treatment with LPS, and decreased levels of reactive oxygen species and nitric oxide. GRo decreased inflammatory cytokines such as nitric oxide synthase and cyclooxygenase-2 induced by LPS. Moreover, GRo increased the expression of HO-1 in a dose dependent manner. Cotreatment of GRo with tin protoporphyrin IX, a selective inhibitor of HO-1, not only inhibited upregulation of HO-1 induced by GRo, but also reversed the anti-inflammatory effect of GRo in LPS treated Raw 264.7 cells. Conclusion: GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.
Kim, Sokho,Oh, Myung-Hoon,Kim, Bum-Seok,Kim, Won-Il,Cho, Ho-Seong,Park, Byoung-Yong,Park, Chul,Shin, Gee-Wook,Kwon, Jungkee The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.4
Background: The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been sufficiently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GRo in vitro using the Raw 264.7 mouse macrophage cell line treated with lipopolysaccharide (LPS), and to clarify the possible mechanism of GRo involving heme oxygenase-1 (HO-1), which itself plays a critical role in self-defense in the presence of inflammatory stress. Methods: Raw 264.7 cells were pretreated with GRo (up to $200{\mu}M$) for 1 h before treatment with 1 mg/mL LPS, and both cell viability and inflammatory markers involving HO-1 were evaluated. Results: GRo significantly increased cell viability in a dose dependent manner following treatment with LPS, and decreased levels of reactive oxygen species and nitric oxide. GRo decreased inflammatory cytokines such as nitric oxide synthase and cyclooxygenase-2 induced by LPS. Moreover, GRo increased the expression of HO-1 in a dose dependent manner. Cotreatment of GRo with tin protoporphyrin IX, a selective inhibitor of HO-1, not only inhibited upregulation of HO-1 induced by GRo, but also reversed the anti-inflammatory effect of GRo in LPS treated Raw 264.7 cells. Conclusion: GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.
Kim, Sokho,Lee, Dongho,Kim, Jae-Kyung,Kim, Jae-Hun,Park, Jong-Heum,Lee, Ju-Woon,Kwon, Jungkee American Chemical Society 2014 Journal of agricultural and food chemistry Vol.62 No.49
<P>The present study investigated the effects of viscothionin, a compound isolated from Korean mistletoe (<I>Viscum album coloratum</I>), on nonalcoholic fatty liver disease (NAFLD) in both in vitro and in vivo models. A connection was discovered between viscothionin and the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, which is involved in lipid metabolism. Viscothionin was shown to significantly attenuate lipid accumulation in HepG2 cells treated with oleic acid, which induces lipid accumulation. Moreover, the phosphorylation of AMPK and acetyl-coenzyme A carboxylase in HepG2 cells was increased by viscothionin treatment. Viscothionin was orally administered to high fat diet-induced obese mice and subsequently histopathological analysis associated with AMPK signaling pathways was evaluated. A significant reduction in the extent of hepatic steatosis was revealed in viscothionin-treated obese mice. Thus, viscothionin mediates its beneficial effects on NAFLD via AMPK signaling pathways, suggesting that it may be a potential target for novel NAFLD treatments.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jafcau/2014/jafcau.2014.62.issue-49/jf503535s/production/images/medium/jf-2014-03535s_0008.gif'></P>
The Functional Possibility of Ubiquitin Proteasome System in Glial Cells for New Treatment Strategy
Sokho Kim,Sehwan Shim,Gee-Wook Shin,Ki-Chang Lee,Min-Su Kim,Nam-Su Kim,Young-Bae Kwon,Jungkee Kwon 한국실험동물학회 2009 Laboratory Animal Research Vol.25 No.3
Neurodegenerative diseases are characterized by the accumulation of misfolded proteins that adversely affect neuronal connectivity and plasticity, and trigger cell death signaling pathways. The ubiquitin proteasome system (UPS) is the main intracellular proteolytic system, responsible for the selective removal of damaged and unfolded proteins. Recently many evidences demonstrated that the UPS function degeneration can enhance the processing of neurodegenerative diseases. In the present study, we have showed the functional possibility of the UPS in vitro at the cellular leveling glial cells. In the highly purified glial cultures, astrocytes and microglia, most of these cells were positive for GFAP and CD11b, a specific marker for astrocytes and microglia, respectively. Ubiquitin and ubiquitin C-terminal hydrolase L1 (UCH-L1) is one of the UPS components. Immunocytochemistry analysis showed the expression of ubiquitin and UCH-L1 in the GFAP and CD11b-immunoreactive cultured cells, respectively. On the basis of this evidence, we first suggest that the UPS might play a role in glial cells, astrocytes and microglia. Although little is known about UPS functions in glial cells, our reports have indicated that UPSmediated neurodegenerative diseases can be investigated for glial proteolytic dysfunction.
Sokho Kim,Ji-Young Na,Ki-Bbeum Song,Dea-Seung Choi,Jong-Hoon Kim,Young-Bae Kwon,Jungkee Kwon 고려인삼학회 2012 Journal of Ginseng Research Vol.36 No.2
The abnormal maturation and ossifi cation of articular chondrocytes play a central role in the pathogenesis of osteoarthritis (OA). Inhibiting the enzymatic degradation of the extracellular matrix and maintaining the cellular phenotype are two of the major goals of interest in managing OA. Ginseng is frequently taken orally, as a crude substance, as a traditional medicine in Asian countries. Ginsenoside Rb₁, a major component of ginseng that contains an aglycone with a dammarane skeleton, has been reported to exhibit various biological activities, including anti-infl ammatory and anti-tumor effects. However, a chondroprotective effect of ginsenoside Rb1 related to OA has not yet been reported. The purpose of this study was to demonstrate the chondroprotective effect of ginsenoside Rb1 on the regulation of pro-infl ammatory factors and chondrogenic genes. Cultured rat articular chondrocytes were treated with 100 μM ginsenoside Rb1 and/or 500 μM hydrogen peroxide (H2O2) and assessed for viability, reactive oxygen species production, nitric oxide (NO) release, and chondrogenic gene expression. Ginsenoside Rb1 treatment resulted in reductions in the levels of pro-infl ammatory cytokine and NO in H₂O₂-treated chondrocytes. The expression levels of chondrogenic genes, such as type Ⅱ collagen and SOX9, were increased in the presence of ginsenoside Rb1, whereas the expression levels of infl ammatory genes related to chondrocytes, such as MMP1 and MMP13, were reduced by approximately 50%. These results suggest that ginsenoside Rb₁ has potential for use as a therapeutic agent in OA patients.