• Journal of Ginseng Research
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• v.37 no.4
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• pp.413-424
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• 2013

Korean Red Ginseng extract (KRGE) is a traditional herbal medicine utilized to prevent endothelium dysfunction in the cardiovascular system; however, its underlying mechanism has not been clearly elucidated. We here examined the pharmacological effect and molecular mechanism of KRGE on apoptosis of human umbilical vein endothelial cells (HUVECs) in a serum-deprived apoptosis model. KRGE protected HUVECs from serum-deprived apoptosis by inhibiting mitochondrial cytochrome c release and caspase-9/-3 activation. This protective effect was significantly higher than that of American ginseng extract. KRGE treatment increased antiapoptotic Bcl-2 and Bcl-$X_L$ protein expression and Akt-dependent Bad phosphorylation. Moreover, KRGE prevented serum deprivation-induced subcellular redistribution of these proteins between the mitochondrion and the cytosol, resulting in suppression of mitochondrial cytochrome c release. In addition, KRGE increased nitric oxide (NO) production via Akt-dependent activation of endothelial NO synthase (eNOS), as well as inhibited caspase-9/-3 activities. These increases were reversed by co-treatment of cells with inhibitors of eNOS and phosphoinositide 3-kinase (PI3K) and pre-incubation of cell lysates in dithiothreitol, indicating KRGE induces NO-mediated caspase modification. Indeed, KRGE inhibited caspase-3 activity via S-nitrosylation. These findings suggest that KRGE prevents serum deprivation-induced HUVEC apoptosis via increased Bcl-2 and Bcl-$X_L$ protein expression, PI3K/Akt-dependent Bad phosphorylation, and eNOS/NO-mediated S-nitrosylation of caspases. The cytoprotective property of KRGE may be valuable for developing new pharmaceutical means that limit endothelial cell death induced during the pathogenesis of vascular diseases.

• Journal of Ginseng Research
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• v.45 no.1
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• pp.119-125
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• 2021

Background: Korean Red Ginseng (KRG) is a natural product with antiinflammatory and anticarcinogenic effects. We have previously reported that the endocrine-disrupting compound bisphenol A (BPA)-induced cyclooxygenase-2 (COX-2) via nuclear translocation of nuclear factor-kappa B (NF-κB) and activation of mitogen-activated protein kinase and promoted the migration of A549. Here, in this study, we assessed the protective effect of KRG on the BPA-induced reactive oxygen species (ROS) and expression of COX-2 and matrix metalloproteinase-9 (MMP-9) in A549 cells. Methods: The effects of KRG on the upregulation of ROS production and COX-2 and MMP-9 expression by BPA were evaluated by fluorescence-activated cell sorting (FACs) analysis, quantitative reverse transcription polymerase chain reaction, and western blotting. Antimigration ability by KRG was evaluated by migration assay in A549 cells. Results: KRG significantly suppressed the BPA-induced COX-2, the activity of NF-κB, the production of ROS, and the migration of A549 cells. These effects led to the downregulation of the expression of MMP-9. Conclusions: Overall, our results suggest that KRG exerts an antiinflammatory effect on BPA-treated A549 cells via the suppression of ROS and downregulation of NF-κB activation and COX-2 expression which leads to a decrease in cellular migration and MMP-9 expression. These results provide a new possible therapeutic application of KRG to protect BPA-induced possible inflammatory disorders.

• Journal of Pharmacopuncture
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• v.24 no.1
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• pp.24-31
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• 2021

Objectives: Accumulation of cellular reactive oxygen species (ROS) leads to oxidative stress. Increased production of ROS, such as superoxide anion, or a deficiency in their clearance by antioxidant defences, mediates cellular pathology. Grewia Spp fruits are a source of bioactive compounds and have notable antioxidant activity. Although the antioxidant capacity of Grewia Spp has been studied, there is very limited evidence that links the antioxidant activities of Grewia bicolor and Grewia flava to the inhibition of free radical formation associated with damage in biological systems. Methods: This study evaluated the protective effects of Grewia bicolor and Grewia flava extracts against free radical-induced oxidative stress and the resulting cytotoxicity effect using HeLa cells. Antioxidant properties determined using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and total phenolic content (TPC) assays showed significantly higher (p < 0.05) antioxidant activity in Grewia flava (ethanol extract) than Grewia flava (water extract) and Grewia bicolor (ethanol and water extracts). Results: Using 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide or MTT assay, cytotoxicity results showed that extracts of Grewia bicolor and Grewia flava were less toxic to HeLa cells at tested concentrations compared to the untreated control. This confirmed the low toxicity of these edible fruits at the tested concentrations in HeLa cells. Furthermore, hydrogen peroxide (H2O2)-induced cell loss was effectively reduced by pre-incubating HeLa cells with Grewia bicolor and Grewia flava extracts, with Grewia flava (ethanol extract) revealing better protection. Conclusion: The effect was speculated to be associated with the higher antioxidant activity of Grewia flava (ethanol extract). Additional studies will warrant confirmation of the mechanism of action of such effects.

• Journal of Ginseng Research
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• v.48 no.4
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• pp.405-416
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• 2024

Background: Hypoxic pulmonary hypertension (HPH) is the main pathological change in vascular remodeling, a complex cardiopulmonary disease caused by hypoxia. Some research results have shown that ginsenoside Rg1 (Rg1) can improve vascular remodeling, but the effect and mechanism of Rg1 on hypoxia-induced pulmonary hypertension are not clear. The purpose of this study was to discuss the potential mechanism of action of Rg1 on HPH. Methods: C57BL/6 mice, calpain-1 knockout mice and Pulmonary artery smooth muscle cells (PASMCs) were exposed to a low oxygen environment with or without different treatments. The effect of Rg1 and calpain-1 silencing on inflammation, fibrosis, proliferation and the protein expression levels of calpain-1, STAT3 and p-STAT3 were determined at the animal and cellular levels. Results: At the mouse and cellular levels, hypoxia promotes inflammation, fibrosis, and cell proliferation, and the expression of calpain-1 and p-STAT3 is also increased. Ginsenoside Rg1 administration and calpain-1 knockdown, MDL-28170, and HY-13818 treatment showed protective effects on hypoxia-induced inflammation, fibrosis, and cell proliferation, which may be associated with the downregulation of calpain-1 and p-STAT3 expression in mice and cells. In addition, overexpression of calpain 1 increased p-STAT3 expression, accelerating the onset of inflammation, fibrosis and cell proliferation in hypoxic PASMCs. Conclusion: Ginsenoside Rg1 may ameliorate hypoxia-induced pulmonary vascular remodeling by suppressing the calpain-1/STAT3 signaling pathway.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.38 no.1
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• pp.15-31
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• 2012

In our previous studies, the antioxidant, anti-aging, and antibacterial activities of Persicaria hydropipier L. extract, and the moisturizing effect of cream containing P. hydropipier extract were investigated. In this study, the cellular protective effects of P. hydropipier extract and isoquercitrin, main component from P. hydropipier in $^1O_2$-induced photohemolysis of human erythrocytes and ultraviolet B (UVB)-exposed HaCaT cells were investigated. Liposomes such as ethosome and elastic liposome for enhanced transdermal delivery were prepared. Size, loading efficiency, stability, and cumulative permeated amounts of ethosomes and elastic liposomes were evaluated. P. hydropipier extract and isoquercitrin showed more prominent cellular protective effect than (+)-${\alpha}$-tocopherol, known as lipid antioxidant at $5{\mu}g/mL$. P. hydropipier extract didn't show any characteristics of cytotoxicity at $50{\mu}g/mL$. When HaCaT cells were exposed to a single large dose ($400mJ/cm^2$) of UVB, the extract protected the cells against UVB radiation in a concentration dependent manner ($12.5{\sim}50{\mu}g/mL$). Cell viability of HaCaT cells exposed to UVB $400mJ/cm^2$ was increased by treatment with P. hydropipier extract or isoquercitrin from 36 % (cell viability of positve control groups) to 90 % (cell viability of P. hydropipier extract or isoquercitrin- treated groups). The size of 0.04 % P. hydropiper extract loaded ethosomes was 173.0 nm and the loading efficiency was 55.58 %. 0.04 % P. hydropiper extract loaded ethosomes were stable with as monodisperse particles for 1 week. The ethosome exhibited more skin permeability than general liposome and ethanol solution. The optimal ratio of lipid to surfactant ($Tego^{(R)}$ care 450) of 0.1 % P. hydropiper extract loaded elastic liposomes was observed to be 95 : 5. Vesicle size of 0.1 % P. hydropiper extract loaded elastic liposome was 176.5 nm. The deformability index of the elastic liposome was 16.4. The loading efficiency was 68.8 %. The elastic liposome containing P. hydropiper extract showed more skin permeability than liposome without surfactant ($Tego^{(R)}$ care 450).

• Journal of the Society of Cosmetic Scientists of Korea
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• v.39 no.4
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• pp.259-269
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• 2013

In this work, licorice extracts were prepared using various extraction conditions such as extraction solvent, temperature, and time from Glycyrrhiza uralensis (G. uralensis) produced in Korea and China and Glycyrrhiza glabra (G. glabra) in Uzbekistan. The optimum extraction condition was selected from the extraction yields and antioxidative activities of extracts. Korea licorice extracts showed the highest free radical (1,1-diphenyl-2-picrylhydrazyl, DPPH) scavenging activity (46.05%) under the extraction condition of 85% ethanol at $60^{\circ}C$ for 6 hours. The prominent ROS (reactive oxygen species) scavenging activity using luminol-dependent chemiluminescence assay and the cellular protective effect against $^1O_2$ induced cellular membrane damage were also shown from the extracts obtained from the same condition. Especially, Korea G. uralensis extracts exhibited the higher prominent protective effect (${\tau}_{50}$ = 116.4 min) than (+)-(+)-${\alpha}$-tocopherol (${\tau}_{50}$ = 28.5 min) and the extraction yield of Korea licorice extract was 18.75%, which is 1.2 times and 2.5 times higher than that of Uzbekistan and China, respectively. These results indicate that the extraction condition of 85% ethanol at $60^{\circ}C$ for 6 hours is optimal to prepare licorice extracts, which can be applicable as anti-oxidative cosmetic materials.

• Journal of Ginseng Research
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• v.41 no.2
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• pp.169-179
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• 2017

Background: Ginsenosides are the main pharmacological components of Panax ginseng root, which are thought to be primarily responsible for the suppressing effect on oxidative stress. Methods: 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and oxygen radical absorption capacity were applied to evaluate the antioxidant activities of the ginsenosides. Human embryonic kidney 293 (HEK-293) cells were incubated with ginsenosides extracted by pulsed electric field (PEF) and solvent cold soak extraction (SCSE) for 24 h and then the injury was induced by $40{\mu}M$ $H_2O_2$. The cell viability and surface morphology of HEK-293 cells were studied using MTS assay and scanning electron microscopy, respectively. Dichloro-dihydro-fluorescein diacetate fluorescent probe assay was used to measure the level of intracellular reactive oxygen species. The intracellular antioxidant activities of ginsenosides were evaluated by cellular antioxidant activity assay in HepG2 cells. Results: The PEF extracts displayed the higher 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and stronger oxygen radical absorption capacity (with an oxygen radical absorption capacity value of $14.48{\pm}4.04{\mu}M\;TE\;per\;{\mu}g/mL$). The HEK-293 cell model also suggested that the protective effect of PEF extracts was dose-dependently greater than SCSE extracts. Dichloro-dihydro-fluorescein diacetate assay further proved that PEF extracts are more active (8% higher than SCSE extracts) in reducing intracellular reactive oxygen species accumulation. In addition, scanning electron microscopy images showed that the HEK-293 cells, which were treated with PEF extracts, maintained more intact surface morphology. Cellular antioxidant activity values indicated that ginsenosides extracted by PEF had stronger cellular antioxidant activity than SCSE ginsenosides extracts. Conclusion: The present study demonstrated the antioxidative effect of ginsenosides extracted by PEF in vitro. Furthermore, rather than SCSE, PEF may be more useful as an alternative extraction technique for the extraction of ginsenosides with enhanced antioxidant activity.

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.1
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• pp.21-28
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• 2017

Background: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes. Method: The following groups were used for experimentation: control, cells were incubated under normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) without propofol; hydrogen peroxide ($H_2O_2$), cells were exposed to $H_2O_2$ ($300{\mu}M$) for 2 h; propofol preconditioning (PPC)/$H_2O_2$, cells pretreated with propofol ($100{\mu}M$) for 2 h were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)/PPC/H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis. Results: Cell viability decreased significantly in the $H_2O_2$ group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased $H_2O_2$-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the $PPC/H_2O_2$ group compared to that in the $H_2O_2$ group as demonstrated by western blot analysis and autophagosome staining. Conclusion: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.48 no.2
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• pp.157-167
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• 2022

In this study, we investigated the effects of heptapeptide on cellular activation and inhibition of cellular damage induced by photoaging condition in NIH3T3 fibroblasts. Cell proliferation and extracellular matrix (ECM) expression were induced by heptapeptide. The reduced cell viability under photoaging condition through ultraviolet A (UVA) irradiation was increased by heptapeptide. And UVA-induced apoptosis, matrix metalloproteinases-1 (MMP-1) expression, and reactive oxygen species (ROS) level were decreased by heptapeptide. In addition, the inhibition of transforming growth factor-β (TGF-β)/smad signaling under UVA irradiation which resulting in reduction of ECM expression was also recovered by heptapeptide. We also tested the effect of heptapeptide under another photoaging condition through heat shock, and pre-treatment of heptapeptide prevented the phosphorylation of mitogen-activated protein kinase (MAPK) and MMP-1 expression induced by heat shock. From these results, it has been shown that the heptapeptide has protective effects on fibroblasts through the up-regulation of cellular activity and through the decreasing of intracellular ROS level induced by UVA irradiation or heat shock. It is expected that the dermal protection effect of heptapeptide can be applied as a new cosmetic material in the future.

• Journal of The Korean Dental Society of Anesthesiology
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• v.14 no.1
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• pp.41-47
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• 2014

Background: Autophagy is a self-eating process that is important for balancing sources of energy at critical times in development and in response stress. Autophagy also plays a protective role in removing clearing damaged intracellular organelles and aggregated proteins as well as eliminating intracellular pathogens. The purpose of the present study was to examine the protective effect of propofol against hypoxic damage using keratinocytes. Methods: Human keratinocytes (HaCaT cells) were obtained from the American Type Culture Collection. Propofol which were made by dissolving them in DMSO were kept frozen at $-4^{\circ}C$ until use. The stock was diluted to their concentration with DMEM when needed. Prior to propofol treatment cells were grown to about 80% confluence and then exposed to propofol at different concentrations (0, 25, 50, 75, $100{\mu}M$) for 2 h pretreatment. Cell viability was measured using a quantitative colorimetric assay with thiazolyl blue tetrazolium bromide (MTT assay), and fluorescence microscopy and western blot analysis were used for evaluation of autophagy processes. Results: The viability of propofol-treated HaCaT cells was increased in a dose-dependent manner. Propofol did not show any significant toxic effect on the HaCaT cells. The autophagy inhibitor, 3-methyladenine, reduced cell viability of hypoxia-injured HaCat cells. Fluorescence microscopy and western blot analysis showed propofol induce autophagy pathway signals. Conclusions: Propofol enhanced viability of hypoxia-injured HaCaT cells and we suggest propofol has cellular protective effects by autophagy signal pathway activation.