• Journal of Ginseng Research
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• v.16 no.2
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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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• v.63 no.4
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• pp.413-420
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• 2020

We studied the effects of the extract of aerial parts of hydroponically cultured ginseng (HGE) on alcohol-induced liver damage (AILD) in mice. AILD was induced by the oral administration of ethanol (EtOH) (25%; 5 g/kg body weight) for seven days in the study as well as EtOH-only groups. However, HGE (4 and 12 mg/kg) was orally administered (once daily for ten consecutive days) only to the study group, three days prior to the EtOH treatment. The HGE-treated group showed significantly lower levels of alanine aminotransferase and aspartate aminotransferase than the EtOH-only group. In addition, HGE administration decreased the level of serum lactate dehydrogenase, a known marker of liver damage. The effect of HGE on AILD was found to be dose dependent, and the consecutive administration of HGE showed no side effects in mice. Our study indicates that HGE treatment can potentially reduce oxidative stress and toxicity in the liver of alcohol-treated mice and that HGE can be a useful therapeutic agent for alcohol-induced hepatotoxicity. Additionally, a simple and efficient high-performance liquid chromatography-ultraviolet detection method was developed for determining the contents of four major ginsenosides in HGE. The aerial parts of hydroponically cultured ginseng were extracted using 70% fermented ethanol, and the contents of ginsenosides F5, F3, F1, and F2 in HGE were found to be 2.5, 4.4, 1.4, and 23.3 mg/g, respectively.

• Journal of Ginseng Research
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• v.33 no.4
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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.

• Journal of radiological science and technology
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• v.27 no.3
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• pp.43-50
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• 2004

The effects of ginseng extracts on liver damage induced by high energy x-ray were studied. To one group of ICR male mice were given white(50 mg/kg/day for 7 days, orally) and fermenta ginseng extracts(500 mg/kg/day for 7 days, orally)before irrdiation. To another group were irradiated by 5 Gy dose of high energy x-ray. Contrast group were given with saline(0.1 ml). This study also investigated the effect between MDA, protein content and ginseng extracts on hepatic damage. This study measured the level of MDA(malondialdehyde), protein content in liver tissue. Administrating orally white (50 mg/kg/day for 7 days, orally)and fermenta ginseng extracts(500 mg/kg/day), the level of MDA were generally decreased and the inhibition was increased. And the protein contents were identical with control group. After irradiation, the protein contents were increased and MDA(malondialdehyde) was increased. Therefore, ginseng extracts increased antioxidative enzyme activity. And We know that the antioxidatant effect of extracts from white and fermenta ginseng protect radiation damage by direct antioxidant effect involving SOD, CAT, GPX. It was included that ginsengs can protect against the lipid peroxidation in radiation damage through its antioxidatant properties.

• Journal of radiological science and technology
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• v.27 no.2
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• pp.35-43
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• 2004

Radioprotective effects of ginseng extracts on liver damage induced by high energy x-ray were studied. To one group of ICR male mice were given white(50 mg/kg/day for 7days, orally) and fermenta ginseng extracts(500 mg/kg/day for 7days, orally) before irrdiation. To another group were irradiated by 5 Gy dose of high energy x-ray. Contrast group were given with saline(0.1 ml). This study also investigated the radioprotective effect between SOD, CAT, hydrogen peroxide and ginseng extracts on hepatic damage. This study measured the level of superoxide dismutase(SOD), catalase(CAT), hydrogen peroxide($H_2O_2$) in liver tissue. Administrating orally white (50 mg/kg/day for 7days, orally) and fermenta ginseng extracts(500 mg/kg/day), the activity of SOD, CAT were generally increased and the hydrogen peroxide($H_2O_2$) was decreased. After irradiation, the activity of SOD, CAT were generally decreased and the hydrogen peroxide($H_2O_2$) was increased. Therefore, ginseng extracts increased antioxidative enzyme activity. And We know that the antioxidatant effect of extracts from white and fermenta ginseng protect radiation damage by direct antioxidant effect involving SOD, CAT. It was included that ginseng can protect against radiation damage through its antioxidatant properties.

• Journal of Ginseng Research
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• v.36 no.3
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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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• v.34 no.1
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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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• v.39 no.4
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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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• v.41 no.3
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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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• v.46 no.2
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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.