• Journal of Ginseng Research
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• 제16권2호
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• pp.129-137
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• 1992

This study was carried out to investigate the localization of lipids and lipase activity with lipid staining and cytochemical technique in endosperm cells of Panax ginseng C.A. Meyer seed. In endosperm cells of indehiscent seed, protein bodies facing the umbiliform layer are different in electron density during the various degraded processes. Gradually, protein matrix near the cell wall was lysed and electron lucent inclusions appeared on umbiliform layer. The protein body with high electron density and the spherosome with low electron density were observed in endosperm cells. As a result of lipid staining, electron density of spherosome is more intense than those of the protein matrix within the protein body in endosperm cells of indehiscent seed. Free spherical spherosomes within the umbiliform layer have a high electron density. The spherical spherosomes were more electron densed and were uniform in comparison with the cytoplasmic proteinaceous granules in endosperm cells of seed with red seed coat. The major component of spherosome was determined to be lipid. Lipase activity occurs in the spherosome and near the endosperm cell wall facing the umbiliform layer. Cytochemical reaction products of lipase were observed in the spherosome membrane and in the inner regions of spherosome. After protein bodies were digested, lipase activities were observed in free spherosomes and near the cell wall of endosperm cells. Umbiliform layer composing of fibrillized wall and digested materials of the endosperm cell showed a little lipase reaction products.

• Journal of Applied Biological Chemistry
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• 제63권4호
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• pp.413-420
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• 2020

알코올성 간손상을 유발한 마우스 모델에서 새싹인삼 지상부 추출물(HGE)의 간 보호 효과를 확인하였다. 알코올성 간손상 모델은 25% 알코올을 마우스에 5 g/kg의 농도로 경구 투여하여 이루어졌고, HGE를 투여한 군에는 알코올을 투여하기 3일전부터 경구투여를 시작하여 10일간 마우스 개체 당 4와 12 mg/kg의 농도로 경구투여 하였다. HGE를 투여한 그룹에서는 알코올만 처리한 대조군에 비해 AST 및 ALT 수치가 농도의존적으로 낮아진 것을 확인하였다. 또한, 간손상에 의해 증가된 LDH 수치는 대조군과 유사하게 감소하였다. 새싹인삼 지상부 추출물로 부터 ginsenoside F5, F3, F1, 및 F2의 정량분석 결과는 각각 2.5, 4.4, 1.4, 및 23.3 mg/g으로 확인하였다.

• Journal of Ginseng Research
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• 제33권4호
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• pp.294-304
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• 2009

Ginsenosides are among the most well-known traditional herbal medicines frequently used for the treatment of various symptoms in South Korea. The neuroprotective effects of ginsenoside $Rg_3$ (G-$Rg_3$) on cholesterol-oxide-(CO)-induced neurotoxicity were investigated through the analyses of rat brains. The recently accumulated reports show that ginseng saponins (GTS), the major active ingredients of Panax ginseng, have protective effects against neurotoxin insults. In the present study, the neuroprotective effects of G-$Rg_3$ on CO-induced hippocampal excitotoxicity were examined in vivo. The in-vitro studies using rat cultured hippocampal neurons revealed that G-$Rg_3$ treatment significantly inhibited CO-induced hippocampal cell death. G-$Rg_3$ treatment not only significantly reduced CO-induced DNA damage but also attenuated CO-induced apoptosis. The in-vivo studies that were conducted revealed that the intracerebroventricular (i.c.v.) pre-administration of G-$Rg_3$ significantly reduced i.c.v. CO-induced hippocampal damage in rats. To examine the mechanisms underlying the in-vitro and in-vivo neuroprotective effects of G-$Rg_3$ against CO-induced hippocampal excitotoxicity, the effect of G-$Rg_3$ on the CO-induced elevations of the apoptotic cells in cultured hippocampal cells was examined, and it was found that G-$Rg_3$ treatment inhibited CO-induced apoptosis. The histopathological evaluation demonstrated that G-$Rg_3$ significantly diminished the apoptosis in the hippocampus and also spared the hippocampal CA1, CA3, and dentate gyrus neurons. G-$Rg_3$ also significantly improved the CO-caused behavioral impairment. G-$Rg_3$ itself had no effect, however, on the CO-induced inhibition of succinate dehydrogenase activity (data not shown). These results collectively indicate the G-$Rg_3$-induced neuroprotection against CO in rat hippocampus. With regard to the wide use of G-$Rg_3$, this agent is potentially beneficial in treating CO-induced brain injury.

• 대한방사선기술학회지:방사선기술과학
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• 제27권3호
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• pp.43-50
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• 2004

방사선이 조사된 생쥐 간에서 백삼 및 발효인삼 추출물이 지질과산화, 단백질 함량변화에 어느 정도 영향을 미치는 가에 대한 실험을 하였다. 6 Mev Linac X선이 조사된 간에 대한 방사선 방호효과를 연구하기 위해서 실험동물을 생쥐 5마리를 1군으로 하여 대조군(Co), 방사선조사군(Rad), WGE+Rad투여군, FG+Rad투여군 등 총 4개 군으로 분류하였으며 생쥐를 도살 16시간 전에 절식시킨 후 각 실험군을 경추탈구로 희생시킨 후 분석시료로 사용하였다. 분석시료를 이용하여 각각 2주간 동안의 실험을 한 결과는 아래와 같다. 1. 방사선조사군(Rad)에서는 대조군(Co) 대비 MDA함량은 4시간, 1일, 7일째, 14일째 모두 대조군에 비해 유의성(p<0.01)있게 증가하였다. 반면에 백삼(50 mg/kg/day)과 발효인삼 추출물(500 mg/kg/day)을 방사선 조사전 투여한 실험군에서 각각 방사선조사군(Rad)대비 백삼과 발효인삼추출물 투여군(WG+Rad, FG+Rad)은 1일째 WG+Rad투여군을 제외하고 4시간째, 7일째, 14일째에서 유의성 있게 함량이 감소하였다. 이는 SOD, CAT, GPX, Peroxidase의 항산화효소와 내인성 항산화 물질을 인삼추출물이 활성화시킴으로서 가능하다고 사료되며 발효인삼은 모든 실험군에서 MDA함량을 감소시켜 지질과산화의 억제작용이 있었음을 알 수가 있었다. 2. 방사선조사군(Rad)에서 단백질 함량은 대조군에 비해 4시간, 1일, 7일째 계속 증가하고 특히,14일째 대조군에 비해 유의성(p<0.01)있게 증가하였다. 반면에 방사선조사군(Rad)대비 백삼과 발효인삼추출물 투여군(WG+Rad, FG+Rad)은 4시간째, 1일째에서 FG+Rad투여군이 약간 증가하고 WG+Rad는 거의 함량이 비슷하였으며 7일째, 14일째에서 유의성(p<0.05)있게 함량이 FG+Rad투여군에서 감소하였고 WG+Rad는 거의 함량이 비슷하였다. 이는 방사선 조사에 대한 백삼과 발효인삼추출물이 회복현상을 나타냄을 알 수 가 있다. 본 실험결과로 볼 때 백삼과 발효인삼추출물은 방사선조사에 의해서 생긴 간세포의 장해에 대한 방호효과가 있었으며 이는 인삼추출물의 성분이 항산화효소(SOD, catalase)의 활성도증가와 MDA함량의 감소 및 단백질 함량의 회복을 가져와 결과적으로 방사선 방호효과가 있었음을 알 수가 있었다.

• 대한방사선기술학회지:방사선기술과학
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• 제27권2호
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• pp.35-43
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• 2004

ICR mice(Takeda et al., 1981)계 수컷 쥐 (무게 $20{\sim}30g$)를 균등한 조사야 $20\;cm{\times}20\;cm$ (선량율 200 cGy/min)로 Linac 6Mev X선 치료 장치(NEC model)를 이용하여 각각 5 Gy씩 실온에서 전신조사 하였다. 6 Mev X선이 조사된 간에 대한 방사선 방어효과를 연구하기 위해서 실험동물 생쥐 5마리를 1군으로 하여 대조군(Co), 방사선조사군(Rad), 방사선 조사전 백삼투여군(WG+Rad투여군), 방사선 조사전 발효인삼투여군(FG+Rad투여군) 등 총 4개 군으로 실험군을 분류하였다. 또한, 대조군(Co), 방사선조사군(Rad)은 생리적식염수 0.1 ml/day를 경구투여 하였고, FG+Rad투여군은 방사선조사 전 7일 동안 발효인삼을 500 mg/kg/day로 생쥐에 경구 투여하였다. 그리고, WG+Rad투여군은 방사선조사 전 7일 동안 백삼을 50 mg/kg/day로 생쥐에 경구 투여하고 생쥐를 도살 16시간 전에 절식시킨 후 각 실험군을 경추탈구로 희생시키고 분석시료로 사용하였다. 생쥐 간에서의 황산화 효소(SOD, catalase) 활성도 변화, 과산화수소 함량변화를 생쥐의 인삼 전 처리 효과를 통해서 방사선 장해에 대한 발효인삼 및 백삼성분이 방어효과에 미치는 영향을 예측하기 위해 전신 X선 조사 후 2주간 연구한 결론은 다음과 같다. 1.방사선조사군(Rad)에서는 대조군(Co)에 비해 SOD, CAT의 효소활성이 감소하였다. 반면에 백삼(50 mg/kg/day)과 발효인삼 추출물(500 mg/kg/day)을 방사선 조사전 투여한 실험군에서 각각 방사선 조사군(Rad)에 비해 효소 활성도가 증가하는 경향을 보였다. 2. 방사선조사군(Rad)에서 과산화수소의 함량은 대조군(Co)에 비해 유의성 있게 증가하였다. 반면에 백삼과 발효인삼 추출물을 방사선 조사전 투여한 실험군에서는 방사선조사군(Rad)에 비해 과산화수소의 함량 생성이 유의성 있게 억제되였다. 3. 본 연구 결과로 볼 때 백삼과 발효인삼추출물은 방사선조사에 의해서 생긴 간세포의 장해에 대한 방어효과가 있었다. 이는 인삼추출물의 성분이 항산화효소(SOD, catalase)의 활성도증가와 과산화수소함량의 감소를 가져와 결과적으로 방사선 방어효과가 나타냄을 알 수가 있었다.

• Journal of Ginseng Research
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• 제36권3호
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• pp.248-255
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• 2012

Potential antioxidant effect of processed ginseng (sun ginseng, SG) on oxidative stress generated by tert-butyl hydroperoxide (t-BHP) was investigated in HepG2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) leakage test demonstrated that SG dose-dependently prevents a loss of cell viability against t-BHP-induced oxidative stress. Also, SG treatment dose-dependently relieved the increment of activities of hepatic enzymes, such as aspartate aminotrasferase and alanine aminotransferase, and lipid peroxidation mediated by t-BHP treatment in HepG2 cells. SG increased the gene expression of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. However, high dose of SG treatment caused decrease in mRNA level of glutathione peroxidase as compared to low dosage of SG-treated cells. The gene expression of glutathione reductase was found to be slightly increased by SG treatment. In addition, SG extract attributed its hepaprotective effect by inducing the mRNA level of bcl-2 and bcl-xL but reducing that of bax. But, the gene expression of bad showed no significant change in SG-treated HepG2 cells. These findings suggest that SG has hepatoprotective effect by showing reduction of LDH release, activities of hepatic enzymes and lipid peroxidation and regulating the gene expression of antioxidant enzymes and apoptosis-related molecules against oxdative stress caused by t-BHP in HepG2 cells.

• Journal of Ginseng Research
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• 제34권1호
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• pp.51-58
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• 2010

This study compared the effects of black, white, and red ginseng extracts (WGE, RGE, BGE, 200 mg/kg, p.o.) on learning and memory deficits associated with scopolamine treatment (SCOP, 2 mg/kg, i.p.). Tacrine (THA, 10 mg/kg, p.o.) was used as a positive control. Ginseng significantly reversed SCOP-induced memory impairment in the passiveavoidance test and also reduced escape latency in training trials of the Morris water maze test. The increased acetylcholinesterase (AChE) activity produced by SCOP was significantly inhibited by WGE and RGE (p<0.001). SCOP administration had no effect on choline acetyltransferase (ChAT) activity, but RGE and BGE significantly increased ChAT activity (p<0.05). SCOP administration increased oxidative damage in the brain. Treatment of amnesic mice with ginseng extracts decreased malondialdehyde (MDA) levels and restored superoxide dismutase (SOD) and catalase (CAT) activity to control levels. These results suggest that black ginseng enhances cognitive activity by regulation of cholinergic enzymes and antioxidant systems.

• Journal of Ginseng Research
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• 제39권4호
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• pp.322-330
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• 2015

Background: UV-irradiated keratinocytes secrete various proinflammatory cytokines. UV-induced skin damage is mediated by growth factors and proinflammatory cytokines such as granulocyte macrophage colony stimulating factor (GM-CSF). In a previous study, we found that the saponin of Korean Red Ginseng (SKRG) decreased the expression of GM-CSF in UVB-irradiated SP-1 keratinocytes. In this study, we attempted to find the inhibitory mechanism of SKRG on UVB-induced GM-CSF expression in SP-1 keratinocytes. Methods: We investigated the inhibitory mechanism of SKRG and ginsenosides from Panax ginseng on UVB-induced GM-CSF expression in SP-1 keratinocytes. Results: Treatment with SKRG decreased the expression of GM-CSF mRNA and protein induced by irradiation of UVB in SP-1 keratinocytes. The phosphorylation of ERK was induced by UVB at 10 min, and decreased with SKRG treatment in SP-1 keratinocytes. In addition, treatment with SKRG inhibited the UVB-induced phosphorylation of epidermal growth factor receptor (EGFR), which is known to be an upstream signal of ERK. From these results, we found that the inhibition of GM-CSF expression by SKRG was derived from the decreased phosphorylation of EGFR. To identify the specific compound composing SKRG, we tested fifteen kinds of ginsenosides. Among these compounds, ginsenoside-Rh3 decreased the expression of GM-CSF protein and mRNA in SP-1 keratinocytes. Conclusion: Taken together, we found that treatment with SKRG decreased the phosphorylation of EGFR and ERK in UVB-irradiated SP-1 keratinocytes and subsequently inhibited the expression of GM-CSF. Furthermore, we identified ginsenoside-Rh3 as the active saponin in Korean Red Ginseng.

• Journal of Ginseng Research
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• 제41권3호
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• pp.316-325
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• 2017

Background: Ginseng essence (GE) is a formulation comprising four medicinal and edible herbs including ginseng (Panax ginseng), American ginseng (Panax quinquefolius), lotus seed (Nelumbo nucifera), and lily bulb (Lilium longiflorum). This study was aimed at investigating the hepatoprotective effect of GE against carbon tetrachloride ($CCl_4$)-induced liver injury in rats. Methods: We treated Wistar rats daily with low, medium, and high [0.625 g/kg body weight (bw), 1.25 g/kg bw, and 3.125 g/kg bw, respectively] doses of GE for 9 wk. After the 1st wk of treatment, rats were administered 20% $CCl_4$ (1.5 mL/kg bw) two times a week to induce liver damage until the treatment ended. Results: Serum biochemical analysis indicated that GE ameliorated the elevation of aspartate aminotransferase and alanine aminotransferase and albumin decline in $CCl_4$-treated rats. Moreover, $CCl_4$-induced accumulation of hepatic total cholesterol and triglyceride was inhibited. The hepatoprotective effects of GE involved enhancing the hepatic antioxidant defense system including glutathione, glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase, and catalase. In addition, histological analysis using hematoxylin and eosin and Masson's trichrome staining showed that GE inhibited $CCl_4$-induced hepatic inflammation and fibrosis. Furthermore, immunohistochemical staining of alpha-smooth muscle actin indicated that $CCl_4$-triggered activation of hepatic stellate cells was reduced. Conclusion: These findings demonstrate that GE improves $CCl_4$-induced liver inflammation and fibrosis by attenuating oxidative stress. Therefore, GE could be a promising hepatoprotective herbal formulation for future development of phytotherapy.

• Journal of Ginseng Research
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• 제46권2호
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• pp.275-282
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• 2022

Background: Stroke is a neurological disorder characterized by brain tissue damage following a decrease in oxygen supply to brain due to blocked blood vessels. Reportedly, 80% of all stroke cases are classified as cerebral infarction, and the incidence rate of this condition increases with age. Herein, we compared the efficacies of Korean White ginseng (WG) and Korean Red Ginseng (RG) extracts (WGex and RGex, respectively) in an ischemic stroke mouse model and confirmed the underlying mechanisms of action. Methods: Mice were orally administered WGex or RGex 1 h before middle cerebral artery occlusion (MCAO), for 2 h; the size of the infarct area was measured 24 h after MCAO induction. Then, the neurological deficit score was evaluated and the efficacies of the two extracts were compared. Finally, their mechanisms of action were confirmed with tissue staining and protein quantification. Results: In the MCAO-induced ischemic stroke mouse model, WGex and RGex showed neuroprotective effects in the cortical region, with RGex demonstrating superior efficacy than WGex. Ginsenoside Rg1, a representative indicator substance, was not involved in mediating the effects of WGex and RGex. Conclusion: WGex and RGex could alleviate the brain injury caused by ischemia/reperfusion, with RGex showing a more potent effect. At 1,000 mg/kg body weight, only RGex reduced cerebral infarction and edema, and both anti-inflammatory and anti-apoptotic pathways were involved in mediating these effects.