• Journal of Ginseng Research
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• 제43권2호
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• pp.319-325
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• 2019

Background: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$). The aim of the current study was to evaluate the possibility of ginsenoside Rf as an active ingredient of KRG in the inhibition of hypoxia-induced COX-2 via $PPAR{\gamma}$. Methods: The effects of ginsenoside Rf on the upregulation of COX-2 by hypoxia and its antimigration effects were evaluated in A549 cells. Docking of ginsenoside Rf was performed with the $PPAR{\gamma}$ structure using Surflex-Dock in Sybyl-X 2.1.1. Results: $PPAR{\gamma}$ protein levels and peroxisome proliferator response element promoter activities were promoted by ginsenoside Rf. Inhibition of COX-2 expression by ginsenoside Rf was blocked by the $PPAR{\gamma}-specific$ inhibitor, T0070907. The $PPAR{\gamma}$ inhibitor also blocked the ability of ginsenoside Rf to suppress cell migration under hypoxia. The docking simulation results indicate that ginsenoside Rf binds to the active site of $PPAR{\gamma}$. Conclusions: Our results demonstrate that ginsenoside Rf inhibits hypoxia induced-COX-2 expression and cellular migration, which are dependent on $PPAR{\gamma}$ activation. These results suggest that ginsenoside Rf has an antiinflammatory effect under hypoxic conditions. Moreover, docking analysis of ginsenoside Rf into the active site of $PPAR{\gamma}$ suggests that the compound binds to $PPAR{\gamma}$ in a position similar to that of known agonists.

• 한국환경보건학회지
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• 제32권6호
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• pp.566-570
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• 2006

Exposure to ultraviolet B(UVB) radiation causes skin inflammation such as pigmentation and the induction of cyclooxygenase-2(COX-2) gene expression. In this study, we investigated the effect of natural extracts from Tea, EGb 761 and Korean red ginseng(KRG), on the pigmentation and expression of COX-1 and COX-2 mRNA in UVB-irradiated C57BL/6 mice. Before UVB irradiation, the skin color was significantly showed the lightening effect by topical application of natural compounds (p<.05). In the case of UVB irradiated mice, we observed a decrease in pigmentation by compounds (p<.05). In irradiated skin, COX-1 mRNA expression is not changed following UVB irradiation, but COX-2 gene increases. Also, natural compounds lowered mRNA levels of COX-2. Therefore, these results suggest that COX-2 mRNA increases by UVB irradiation. Also, Tea, EGb 761 and KRG as a topical application may inhibit skin pigmentation and modulate COX-2 mRNA level.

• Journal of Ginseng Research
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• 제38권4호
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• pp.256-263
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• 2014

Background: Korean Red Ginseng (KRG) is known to have antianxiety properties. This study was conducted to investigate the anxiolytic effects of KRG extract (KRGE) during ethanol withdrawal (EW) and the involvement of the mesoamygdaloid dopamine (DA) system in it. Methods: Rats were treated with 3 g/kg/d of ethanol for 28 d, and subjected to 3 d of withdrawal. During EW, KRGE (20 mg/kg/d or 60 mg/kg/d, p.o.) was given to rats once/d for 3 d. Thirty min after the final dose of KRGE, anxiety-like behavior was evaluated in an elevated plus maze (EPM), and plasma corticosterone (CORT) levels were determined by a radioimmunoassay (RIA). In addition, concentrations of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the central nucleus of the amygdala (CeA) were also measured by high performance liquid chromatography (HPLC). Results: The EPM test and RIA revealed KRGE inhibited anxiety-like behavior and the over secretion of plasma CORT during EW. Furthermore, the behavioral effect was blocked by a selective DA D2 receptor (D2R) antagonist (eticlopride) but not by a selective DA D1 receptor (D1R) antagonist (SCH23390). HPLC analyses showed KRGE reversed EW-induced decreases of DA and DOPAC in a dose-dependent way. Additionally, Western blotting and real-time polymerase chain reaction (PCR) assays showed that KRGE prevented the EW-induced reductions in tyrosine hydroxylase (TH) protein expression in the CeA and TH mRNA expression in the ventral tegmental area (VTA). Conclusion: These results suggest that KRGE has anxiolytic effects during EW by improving the mesoamygdaloid DA system.

• Journal of Ginseng Research
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• 제47권1호
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• pp.81-88
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• 2023

Background: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. Methods: Research of the respiratory protective effects of KRG extract in a particulate matter (PM; aerodynamic diameter of <4 ㎛) plus diesel exhaust particle (DEP) (PM4+D)-induced airway inflammation model. Nitric oxide production, expression of pro-inflammatory mediators and cytokines, and IRAK-1, TAK-1, and MAPK pathways were examined in PM4-stimulated MH-S cells. BALB/c mice exposed to PM4+D mixture by intranasal tracheal injection three times a day for 12 days at 3 day intervals and KRGE were administered orally for 12 days. Histological of lung and trachea, and immune cell subtype analyses were performed. Expression of pro-inflammatory mediators and cytokines in bronchoalveolar lavage fluid (BALF) and lung were measured. Immunohistofluorescence staining for IRAK-1 localization in lung were also evaluated. Results: KRGE inhibited the production of nitric oxide, the expression of pro-inflammatory mediators and cytokines, and expression and phosphorylation of all downstream factors of NF-κB, including IRAK-1 and MAPK/AP1 pathway in PM4-stimulated MH-S cells. KRGE suppressed inflammatory cell infiltration and number of immune cells, histopathologic damage, and inflammatory symptoms in the BALF and lungs induced by PM4+D; these included increased alveolar wall thickness, accumulation of collagen fibers, and TNF-α, MIP2, CXCL-1, IL-1α, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1α release by associating with IRAK-1 localization was also potently inhibited by KRGE in the lungs of PM4+D-induced airway inflammation model. KRGE suppresses airway inflammatory responses, including granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines via inhibition of IRAK-1 and MAPK pathway. Conclusion: Our results indicate the potential of KRGE to serve as an effective therapeutic agent against airway inflammation and respiratory diseases.

• 생명과학회지
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• 제23권2호
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• pp.167-174
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• 2013

Peroxiredoxin 6 (Prx 6)는 티올-특이적 항산화 단백질에 속하는 효소로서 산화적 스트레스로부터 세포를 보호할 뿐만 아니라 과산화물의 환원작용을 촉매한다. 본 연구에서는 인간 Prx 6의 promoter를 이용하여 항산화반응을 유발하는 추출물을 효과적으로 스크리닝하는 새로운 형질전환마우스를 개발하는 최종목적을 달성하기 위한 중간단계로서, hPrx 6/Luc 벡터를 개발하고, 이들 벡터의 안정적 발현과 성공적 반응성을 세포주를 이용하여 확인하고자 하였다. 이를 위해, 인간 Prx 6 promoter를 증폭하여 luciferase cDNA와 결합한 hPrx 6/Luc 벡터를 제조하였으며, 제조된 벡터를 제한효소 절단과 염기서열분석을 통해 확인하였다. hPrx 6/Luc 벡터는 NCI-H460 세포에 transfection한 후 인삼(KWG), 홍삼(KRG), 맥문동(LP), 홍문동(RLP)의 4가지 추출물을 처리하여 luciferase activity를 측정하였다. 그 결과, luciferase activity는 4가지 추출물에 의해 효과적으로 증가하였고, 특히 KRG과 LP를 처리한 그룹이 KWG과 RLP를 처리한 그룹보다 높았다. 또한, luciferase activity는 RLP 농도에 의존적으로 증가하였다. hPrx 6/Luc 벡터와 hPrx 6 mRNA반응의 차이를 비교하기 위해, 4가지 추출물을 처리한 후 hPrx 6 mRNA의 양을 RT-PCR로 분석하였다. 그러나, hPrx 6 mRNA의 양은 비록 고농도의 RLP 추출물에서는 약간의 증가가 관찰되었지만, 대조군에 비하여 4가지 추출물에서 유의적인 차이가 없었다. 한편, 4가지 추출물에 의한 superoxide dismutase (SOD) 활성의 변화는 비록 일부 차이는 있었지만 hPrx 6/Luc 벡터와 유사한 반응을 나타내었다. 따라서, 이러한 결과는 hPrx 6/Luc 벡터는 성공적으로 제조되었고, 세포내에서 안정적으로 발현하면서 항상화물질에 민감하고 정량적으로 반응할 수 있음을 제시하고 있다. 더불어, 이러한 세포주에서 확인결과를 바탕으로 형질전환마우스가 개발된다면, 항산화물질을 정량적으로 스크리닝하는 시스템으로 적용가능성이 매우 높음을 보여주고 있다.