• Proceedings of the SCSK Conference
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• 2003.09a
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• pp.85-96
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• 2003

Normal human skin, constantly challenged by environmental micro-organisms, has an innate ability to fight invading microbes through antimicrobial peptides. These peptides, described in both plant and animal kingdoms are able to inactivate a broad spectrum of micro-organisms. Mammalian defensins constitute one of the most common antimicrobial peptide family. Among the three human beta-defensins hBD1, hBD2 and hBD3 produced in epithelia, only hBD2 and hBD3 are inducible and additionally have been described as expressed by differentiated keratinocytes at site of inflammation and infection. The aims of these studies were to define a cell culture model in which the basal production of hBD could be detected and up-regulated in order to enhance skin auto-protection against micro-organisms. A specific Polymerase Chain Reaction method have been developed for hBD2 and hBD3 mRNA detection in non-differentiated monolayer keratinocytes cell culture. We have been able to demonstrate that in vitro, hBD2 and hBD3 expression in normal human keratinocytes could be detected and enhanced by TNF-alpha and IFN-gamma, in hypercalcic culture conditions. This research opened the possibility of the development of cosmetic active compounds, able to induce the expression of skin natural antibiotic peptides responsible about microflora ecology of the skin.

• Preventive Nutrition and Food Science
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• v.1 no.2
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• pp.256-261
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• 1996

Carotenoids are abundant int he Korean food supply. The intake of foods rich in carotenoids appears to be associated with optimal health, and a reduction in the risk of cancer, cardiovascular disease, macular degeneration and cataract formation. Specific dietary carotenoids may be responsible for these specific protective effects. Hydrocarbon carotenoids such as $\alpha$-,$\beta$-carotenes and lycopene may reduce the risk of cancer and heart disease, whereas oxygenated carotenoids, such as lutein and zeaxanthin, may be important in protection of the eye. Dietary carotenoids, such as lutein, cryptoxanthin, $\alpha$-carotene, $\beta$-carotene and lycopene can be readily obtained from the diet, Green leafy vegetables, such as spinach and broccoli, contain both oxygenated and hydrocarbon carotenoids ; yellow or orange vegetables, such as carrots, have high levels of $\alpha$-carotene and $\beta$-carotene ; and tomatoes contain high amounts of lycopene. Besides being important vitamin A sources, provitamin A carotenoids such as $\alpha$-carotene, $\beta$-carotene and cryptoxanthin, participate in the cell defense systems that are associated with radical quenching. Non-provitamin A carotenoids, such as lutein and lycopene, major carotenoids in human plasma, have also been reported to possess strong antioxidant capability. The alteration of dietary sources of carotenoids can modify their levels in the circulation and target tissues, and thus prevent or delay the onset of these chronic diseases.

• Journal of Radiation Protection and Research
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• v.42 no.4
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• pp.189-196
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• 2017

Background: The effects of radiation on tissues vary depending on the radiation type. In this study, a minipig model was used to compare the effects of ${\beta}$-rays from $^{166}Ho$ and ${\gamma}$-rays from $^{60}Co$ on the skin. Materials and Methods: In this study, the detrimental effects of ${\beta}$- and ${\gamma}$-irradiation on the skin were assessed in minipigs. The histopathological changes in the skin from 1 to 12 weeks after exposure to 50 Gy of either ${\beta}$- (using $^{166}Ho$ patches) or ${\gamma}$- (using $^{60}Co$) irradiation were assessed. Results and Discussion: The skin irradiated by ${\beta}$-rays was shown to exhibit more severe skin injury than that irradiated by ${\gamma}$-rays at 1-3 weeks post-exposure; however, while the skin lesions caused by ${\beta}$-rays recovered after 8 weeks, the ${\gamma}$-irradiated skin lesions were not repaired after this time. The observed histopathological changes corresponded with gross appearance scores. Seven days post-irradiation, apoptotic cells in the basal layer were detected more frequently in ${\beta}$-irradiated skin than in ${\gamma}$-irradiated skin. The basal cell density and skin thickness gradually decreased until 4 weeks after ${\gamma}$- and ${\beta}$- irradiation. In ${\beta}$-irradiated skin lesions, and the density and thickness increased sharply back to control levels by 6-9 weeks. However, this was not the case in ${\gamma}$-irradiated skin lesions. In ${\gamma}$-irradiated skin, cyclooxygenase-2 (COX-2) was shown to be expressed in the epidermis, endothelial cells of vessels, and fibroblasts, while ${\beta}$-irradiated lesions exhibited COX-2 expression that was mostly limited to the epidermis. Conclusion: In this study, ${\beta}$-rays were shown to induce more severe skin injury than ${\gamma}$-rays; however, the ${\beta}$-rays-induced injury was largely repaired over time, while the ${\gamma}$-rays-induced injury was not repaired and instead progressed to necrosis. These findings reveal the differential effects of ${\gamma}$- and ${\beta}$-irradiation on skin and demonstrate the use of minipigs as a beneficial experimental model for studying irradiation-induced skin damage.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.2
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• pp.436-441
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• 2006

Rheumatoid arthritis is a chronic, systemic, and inflammatory autoimmune disorder that affects 1% of the adult population worldwide. Osteoarthritis is a multifactorial disease with high morbidity that is characterized by degradation of the matrix and destruction of articular cartilage. In this study, we examined the inhibition effect of Trachelospermi Caulis on the inflammation($TNF-{\alpha}$, $IL-1{\beta}$, NO), cartilage protection(MMP-13), and cell death in arthritis. RAW 264.7 and SW 1353 cells were cultivated in DMAE(GibcoBRL, USA) with 5% FBS and Fungizone in $37^{\circ}C$, 5% CO2. THP-1 cells were cultivated in RPMI(GibcoBRL, USA) with 5% FBS and Fungizone in $37^{\circ}C$, 5% CO2. Activity of caspase-3, XIAP, Cytochrome C in the cell was examined by using western blot. The results obtained were as Follows; Concentration of nitric oxide in Trachelospermi Caulis treatment group significantly decreased compared with that of non-treatment group (P<0.05). In treated group, Concentration of Trachelospermi Caulis was not significantly associated with cell death. Concentration of $TNF-{\alpha}$ and $IL-1{\beta}$ in Trachelospermi Caulis treatment group decreased significantly compared with that of none treatment group (P<0.05). Relative density of MMP-13 in Trachelospermi Caulis treatment group decreased significantly compared with that of none treatment group and dose-response relationship was observed. After treatment of staurosporin in SW1353 which increases cell death, in Trachelospermi Caulis treated group, the cell death was effectively decreased. In conclusion, these results suggest that Trachelospermi Caulis inhibit inflammation and cell death in arthritis. More researches about effect of Trachelospermi Caulis are considered to need.

• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.1
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• pp.18-26
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• 2015

Akebiae Caulis is a galenical originated from Akebia quinata Decaisne species. It is commonly used in the treatment of oposiuria, inflammation, nociceptive and fever. Here, we investigated the effect of Akebiae Caulis extract (ACE) to protect hepatocyte against the malfunction of mitochondria and apoptosis. Arachidonic acid (AA)+iron promoted excessive reactive oxygen species (ROS) production and exerted a deleterious effect on mitochondria. Treatment with ACE protected hepatocytes from AA+iron-induced cytotoxicity, as shown by alterations in the protein levels related with apoptosis such as poly(ADP-ribose) polymerase, pro-caspase 3, Bcl-XL and Bcl-2. Moreover, AA+iron-induced $H_2O_2$ production, GSH depletion and mitochondrial dysfunction were alleviated by ACE pretreatment. As a potential molecular mechanism for the ACE-mediated cytoprotection, phosphorylation of AMP-activated protein kinase (AMPK), a key regulator in determining cell survival or death, was increased by ACE. Moreover, ACE treatment enhanced inactive phosphorylation of glycogen synthase kinase-$3{\beta}$ ($GSK3{\beta}$), downstream substrate kinase of AMPK. More importantly, ACE prevented a decrease in the $GSK3{\beta}$ phosphorylation derived by AA+iron, which might contribute to mitohondiral protection and cell survival. To further identify essential compounds in Akebiae Caulis for the protection of AA+iron-mediated cytotoxicity, we found that betulin in combination with hederagenin protected from AA+iron-induced mitochondrial dysfunction. Betulin+hederagenin treatment also increased inactive phosphorylation of $GSK3{\beta}$ in common with ACE. These results suggest that ACE protected hepatocytes against oxidative stress and mitochondrial dysfunction, which is mediated with inactive $GSK3{\beta}$ phosphorylation downstream of AMPK.

• Animal cells and systems
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• v.9 no.2
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• pp.101-105
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• 2005

[ ${\beta}ig-h3$ ] is a secretory protein that is induced by $TGF-{\beta}$ and implicated in various disease conditions including fibrosis. We have previously reported that ${\beta}ig-h3$ expression is implicated in astrocyte response to brain injury. In this study, we further investigated potential roles of ${\beta}ig-h3$ protein in the injured central nervous system (CNS). We specifically assessed whether the treatment of microglial cells with ${\beta}ig-h3$ can regulate microglial activity. Microglial cells are the prime effector cells in CNS immune and inflammatory responses. When activated, they produce a number of inflammatory mediators, which can promote neuronal injury. We prepared conditioned medium from the stable CHO cell line transfected with human ${\beta}ig-h3$ cDNA. We then examined the effects of the conditioned medium on the LPS- or $IFN-{\gamma}-mediated$ induction of proinflammatory molecules in microglial cells. Preincubation with the conditioned medium significantly attenuated LPS-mediated upregulation of $TNF-{\alpha},\;IL-1{\beta}$, iNOS and COX-2 mRNA expression in BV2 murine microglial cells. It also reduced $IFN-{\gamma}-mediated$ upregulation of $TNF-{\alpha}$ and COX-2 mRNA expression but not iNOS mRNA expression. Assays of nitric oxide release correlated with the mRNA data, which showed selective inhibition of LPS-mediated nitric oxide production. Although the regulatory mechanisms need to be further investigated, these results suggest that astrocyte-derived ${\beta}ig-h3$ may contribute to protection of the CNS from immune-mediated damage via controlling microglial inflammatory responses.

• The Journal of Korean Physical Therapy
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• v.21 no.2
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• pp.109-116
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• 2009

Purpose: $17\beta$-estradiol is the most active endogenous estrogen, which is related to favorable changes in the plasma lipid profile, to relaxation of the coronary vessels, and to a decrease in platelet aggregation and vascular smooth muscle cell migration. However, although the beneficial effect of estrogens on plasma lipoproteins (ie, lowering low-density lipoprotein and increasing high-density lipoprotein cholesterol) contributes to cardiovascular protection, it does not fully account for the protective effect, particularly in the application of physical therapy, including low frequency electrical stimulation. Methods: The aim of this study was to demonstrate the inhibition of stressors, such as endothelin-1 (ET-1), serotonin (5-hydroxytryptamine, 5-HT), prostaglandin $F2\alpha$ ($PGF2\alpha$), and a protein kinase C (PKC) activator 12-deoxyphorbol 13-isobutyrate (DPB), induced isometric tension by $17\beta$-estradiol in vascular smooth muscle strips, respectively. In addition, the effects of low frequency electrical stimulation at the meridian points (CV-3, -4, Ki-12, SP-6, LR-3, BL-25, -28, -32, -52) on the indirect antihypertensive effect were examined by monitoring the changes in the serum $17\beta$-estradiol concentration in healthy volunteers. Results: Isometric tension analysis showed that the responses of inhibited tension by $17\beta$-estradiol were similar to the same stressors in rat aortic smooth muscle strips. Furthermore, although the continued amplitude modulation (AM) type of electrical stimulation was not increased significantly by electrical stimulation, the current of the frequency modulation (FM) type of low frequency electrical stimulation increased the serum $17\beta$-estradiol concentration in normal volunteers. Conclusion: These results, in part, suggest that $17\beta$-estradiol has the capacity to supress stressor-induced muscle tension, and electrical stimulation, particularly current of the FM type, has a modulatory effect on the sex steroid hormones, particularly $17\beta$-estradiol, in healthy volunteers.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.4
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• pp.460-469
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• 2017

Heat shock proteins (HSPs) are induced as a self-defense mechanism of cells when exposed to various external stresses, such as high fever, infection, free radicals, and heavy metals. They affect the prognosis in the process of tumor formation. HSP is classified into four families: HSP27, HSP60, HSP90, and HSP100, depending on molecular weight. Heat shock protein 90 (HSP90), a molecular chaperone, plays an important role in the cellular protection against various stressful stimuli and in the regulation of cell cycle progression and apoptosis. In the present study, we assessed the differential expression of HSP90 family proteins in non-small cell lung cancer (NSCLC), and the correlation of their expression levels with clinicopathologic factors and patient survival rates. The result of this study can be summarized as follows; $HSP90{\alpha}$ showed higher expression in patients with no lymphovascular invasion (p=0.014). $HSP90{\beta}$ showed a higher expression of squamous cell carcinoma (p=0.003), and an over expression of glucose-related protein (GRP94) was significantly associated with poor differentiation (p=0.048). However, none of the HSP90 proteins showed a significant association with the survival status in patients with NSCLC. This study also indicates that $HSP90{\alpha}$ might contribute more to the carcinogenesis of NSCLC than $HSP90{\beta}$, and GRP94 and isoform selectivity should be considered when HSP90 inhibitors are studied or utilized in the treatment of NSCLC.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.572-582
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• 2023

Background: Free fatty acid-induced lipotoxicity is considered to play an important role in pancreatic β-cell dysfunction. The effect of ginsenosides on palmitic acid-induced pancreatic beta-cells cell death and failure of glucose-stimulated secretion of insulin (GSIS) was evaluated in this study. Methods: Enzyme-linked immunosorbent assay kit for a rat insulin was used to quantify glucose-stimulated insulin secretion. Protein expression was examined by western blotting analysis. Nuclear condensation was measured by staining with Hoechst 33342 stain. Apoptotic cell death was assessed by staining with Annexin V. Oil Red O staining was used to measure lipid accumulation. Results: We screened ginsenosides to prevent palmitic acid-induced cell death and impairment of GSIS in INS-1 pancreatic β-cells and identified protopanaxadiol (PPD) as a potential therapeutic agent. The protection effect of PPD was likely due to a reduction in apoptosis and lipid accumulation. PPD attenuated the palmitic acid-induced increase in the levels of B-cell lymphoma-2-associated X/B-cell lymphoma 2, poly (ADP-ribose) polymerase and cleaved caspase-3. Moreover, PPD prevented palmitic acid-induced impairment of insulin secretion, which was accompanied by an increase in the activation of phosphatidylinositol 3-kinase, peroxisome proliferator-activated receptor γ, insulin receptor substrate-2, serine-threonine kinase, and pancreatic and duodenal homeobox-1. Conclusion: Our results suggest that the protective effect of PPD on lipotoxicity and lipid accumulation induced by palmitic acid in pancreatic β-cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.14
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• pp.5501-5508
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• 2014

Luteolin, 3', 4', 5,7-tetrahydroxyflavone, belongs to a group of naturally occurring compounds called flavonoids that are found widely in the plant kingdom. It possesses many beneficial properties including antioxidant, anti-inflammatory, anti-bacterial, anti-diabetic and anti-proliferative actions. Colorectal cancer (CRC) is a leading cause of cancer related deaths worldwide. Many signaling pathways are deregulated during the progression of colon cancer. In this review we aimed to analyze the protection offered by luteolin on colon cancer. During colon cancer genesis, luteolin known to reduce oxidative stress thereby protects the cell to undergo damage in vivo. Wnt/${\beta}$-catenin signaling, deregulated during neoplastic development, is modified by luteolin. Hence, luteolin can be considered as a potential drug to treat CRC.