• Korean Journal of Food Science and Technology
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• v.43 no.5
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• pp.633-640
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• 2011

After Ganoderma lucidum was cultured in mushroom complete medium (MCM) supplemented with ginseng extract (GE), crude polysaccharide (GL-GE-CP) was fractionated from mycelium. Among GL-GE-CP from mycelium in MCM supplemented with 5, 10, and 15% GE (v/v ratio of MCM to GE), GL-GE-15-CP (15% GE) most significantly enhanced macrophage stimulation and intestinal immune system modulating activity compared with GL-CP in MCM without GE. When GL-GE-15-CP was further fractionated on DEAE-Sepharose CL-6B, GL-GE-15-CP-II displayed more potent activity than subfractions from GL-CP on macrophage stimulation, interleukin-12 production, and intestinal immune system modulation (1.75-, 5.68-, and 1.76-fold, respectively). Anti-metastasis effect against colon 26-M3.1 carcinoma cells was also enhanced by GL-GE-15-CP-II (72.8% inhibition). In addition, GL-GE-15-CP-II contained neutral sugar (83.00%) and uronic acid (9.11%), and consisted of Ara, Man, Gal and Glc (molar ratio of 0.39:0.50:0.75:1.00). Furthermore, GE supplementation helped to enhance the immunomodulation in G. lucidum, and it is assumed that neutral polysaccharides play an important role.

• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.172-183
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• 1999

Background: Nitric oxide is a short-lived effector molecule derived from L-arginine by the nitric oxide synthase(NOS). Nitric oxide plays a role in a number of physiologic and pathophysiologic functions including host defense, edema formation, and regulation of smooth muscle tone. Some kinds of cells including macrophage are known to produce large quantities of nitric oxide in response to inflammatory stimuli such as interleukin-$1\beta$(IL-$1\beta$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), interferon-$\gamma$(IFN-$\gamma$) and lipopolysaccharide(LPS). Reactive oxygen species are also known to be important in the pathogenesis of acute cell and tissue injury such as acute lung injury model Methods: Using the RA W264.7 cells, we have examined the ability of oxidant hydrogen peroxide($H_2O_2$) to stimulate nitric oxide production and inducible NOS mRNA expression. Also, we have examined the effects of NOS inhibitors and antioxidants on $H_2O_2$ induced nitric oxide production. Results: Stimulation of RAW264.7 cells with combinations of 100 ng/ml IL-$1\beta$, 100 ng/ml TNF-$\alpha$, and 100 U/ml IFN-$\gamma$ or 100 U/ml IFN-$\gamma$ and $1{\mu}g/ml$ LPS induced the synthesis of nitric oxide as measured by the oxidation products nitrite($NO_2^-$) and nitrate($NO_3^-$). Addition of $250 {\mu}M-2$ mM $H_2O_2$ to the cytokines significantly augmented the synthesis of $NO_2^-$ and $NO_3^-$(p<0.05). When cells were incubated with increasing concentrations of $H_2O_2$ in the presence of IL-$1\beta$, TNF-$\alpha$ and IFN-$\gamma$ at constant level, the synthesis of $NO_2^-$ and $NO_3^-$ was dose-dependently increased(p<0.05). $N^G$-nitro-L-arginine methyl ester(L-NAME), dose dependently, significantly inhibited the formation of $NO_2^-$ and $NO_3^-$ in cells stimulated with LPS, IFN-$\gamma$ and $H_2O_2$ at constant level(p<0.05). Catalase significantly inhibited the $H_2O_2$-induced augmentation of cytokine-induced $NO_2^-$ and $NO_3^-$ formation(p<0.05). But, boiled catalase did not produce a significant inhibition in comparison with the native enzyme. Another antioxidant 2-mercaptoethanol and orthophenanthroline dose-dependently suppressed $NO_2^-$ and $NO_3^-$ synthesis(p<0.05). Northern blotting demonstrated that H:02 synergistically stimulated the cytokine-induced iNOS mRNA expression in RA W264.7. Conclusion: These results suggest that $H_2O_2$ contributes to inflammatory process by augmenting the iNOS expression and nitric oxide synthesis induced by cytokines.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.7
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• pp.929-937
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• 2016

The purpose of this study was to investigate the effect of Acanthopanax senticosus extract (ASE) (ethanol : DW=1:1, v/v) on inhibition of type 2 diabetes using an OLETF rat model via regulation of HbA1c and AGEs levels. Supplementation with ASE 0.1% and 0.5% effectively lowered levels of glucose, insulin, oral glucose tolerance test, and Homa-insulin resistance, suggesting reduced insulin resistance. Blood levels of HbA1c and AGEs were significantly reduced in a dose-dependent manner. As oxidative stress plays a key role in accelerating production of HbA1c and AGEs, which worsen symptoms of type 2 diabetes, levels of malonaldehyde and pro-inflammatory cytokines were measured. Lipid peroxidation in both blood and liver tissues was significantly reduced, and induction of pro-inflammatory cytokines interleukin-${\beta}$ and tumor necrosis factor-${\alpha}$, which elevate production of HbA1c and AGEs, was inhibited (P<0.05). To evaluate the possible cellular events after AGEs receptor activation, genetic expression of protein kinase C (PKC)-${\delta}$ and transforming growth factor (TGF)-${\beta}$ was measured by real-time polymerase chain reaction. Supplementation with both ASE 0.1% and 0.5% significantly inhibited mRNA expression of PKC-${\delta}$ and TGF-${\beta}$, indicating that ASE may have beneficial effects on preventing insulin-resistant cells or tissues from progressing to diabetic complications. Taken together, ASE has potential to improve type 2 diabetes by inhibiting insulin resistance and protein glycosylation, including production of HbA1c and AGEs. Anti-oxidative activities of ASE are a main requisite for reducing production of HbA1c and AGEs and are also related to regulation of the PKC signaling pathway, resulting in suppression of TGF-${\beta}$, which increases synthesis of collagen, prostaglandin, and disease-related proteins.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.7
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• pp.949-955
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• 2011

[ ${\beta}$ ]Glucan is a polysaccharide expressed on the cell walls of fungi. It is known that ${\beta}$-glucan is recognized by a family of C-type lectin receptors, dectin-1, which is expressed mainly on myeloid immune cells, including macrophages, neutrophils and dendritic cells. Raw 264.7 cells were treated with ${\beta}$-glucan from Schizophyllum commune. ${\beta}$-Glucan was not cytotoxic up to 400 ${\mu}g$/mL as measured by MTT assay. To measure the activity of macrophages, NO and TNF-${\alpha}$ assays were performed in Raw 264.7 cells. Treatment with ${\beta}$-glucan for 24 hr significantly increased production of NO and TNF-${\alpha}$ compared with control groups (p<0.05), indicating activation of macrophages. To measure inhibition of breast cancer cell proliferation, MTT assay was performed in MDA-MB-231 cells. Cell viability was significantly decreased in the group treated with 400 ${\mu}g$/mL of ${\beta}$-glucan for 48 hr (p<0.05) compared to the control group. However, tumor volume was decreased in the groups administered 200 ${\mu}g$ of ${\beta}$-glucan/mouse compared to the control group. These results indicate that ${\beta}$-glucan inhibits breast cancer cell growth through the induction of apoptosis.

• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.9
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• pp.1126-1135
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• 2008

This study was carried out to investigate the anti-oxidative and anti-inflammatory actions of genistein in BALB/c mice injected with lopopolysaccharide (LPS), called endotoxin. Mice (10 weeks of age) weighing approximately 20 g were divided into 4 groups. Endotoxin shock was induced by intraperitoneal injection of LPS (100 mg/kg BW). LPS and genistein+LPS groups were injected with LPS 30 min after phosphate buffered saline (PBS) solution and genistein (200 mg/kg BW) injections, respectively. Genistein group was injected with genistein, followed by PBS, while PBS group received two injections of PBS. Superoxide anion generation of peritoneal macrophage cells was significantly (p<0.05) lower in the genistein+LPS group than in the LPS injection group at 8 h after intraperitoneal injection, while SOD activity was significantly higher in genistien+LPS group than LPS group. Tumor necrosis factor-$\alpha$ levels of plasma were significant lower (p<0.05) in the genistein+LPS injection group than LPS group at 8 h after intraperitoneal injection. Plasma TBARS was lower in genistein+LPS group than LPS group, while hepatic TBARS were not different among groups. Hepatic glutathione concentrations and antioxidant enzyme activities were ignificantly higher in the genistein+LPS group than in the LPS group at 1 h and 8 h after intraperitoneal injection. Nuclear factor-kappa B (NF-${\kappa}B$) transactivation was significantly (p<0.05) inhibited in LPS group. These results demonstrate genistein may ameliorate inflammatory diseases through inhibition of NF-${\kappa}B$ transactivation and oxidative stress, which may be mediated partially by anti-oxidative effect of genistein.

• Tuberculosis and Respiratory Diseases
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• v.58 no.5
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• pp.480-489
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• 2005

Background : Dysregulation of apoptosis plays an important role in carcinogenesis, tumor progression, and resistance to chemotherapy. X-linked inhibitor of apoptosis (XIAP) is considered to be the most potent caspase inhibitor of all known IAP (inhibitor of apoptosis) family members. This study was designed to assess the pattern of expression and the prognostic value of XIAP in radically resected non-small cell lung carcinoma (NSCLC) patients. Method : The expression of XIAP and its relationship with clinicopathologic parameters (patient age, TNM stage, TNM-pT, TNM-pN, histologic type, VEGF expression, microvessel density, PCNA index) and overall survival were analysed with formalin-fixed, paraffin-embedded blocks from eighty cases of NSCLC. In addition, the apoptotic index (AI) was also assessed. Results : In a regard to histologic type, squamous cell carcinoma (SCC) showed XIAP expression in 91.3%(42/46) and adenocarcinoma (AC) in 61.8%(21/34). The difference was significant(p=0.001). There was no correlation between XIAP expression and other parameters. In the group of AC, XIAP expression showed the signifcant correlation with older age group ${\geq}58years$ and VEGF expression(p=0.028, p=0.014, respectively). The AI in the group with or without XIAP expression were $2.5{\pm}4.9%$ and $18.5{\pm}28.9%$, respectively(p=0.001). Both groups just aforementioned showed no significant difference in median survival time (42.5 months, 29.8 months, respectively). Conclusion : This study suggests that the XIAP expression in NSCLCs could have relation to inhibition of apoptosis, and show differential expression according to histologic type. However, its prognostic role during the progression of NSCLC needs to be further defined.

• Radiation Oncology Journal
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• v.15 no.3
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• pp.175-186
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• 1997

Purpose : To evaluate the qualitative immunologic changes by ionizing radiation. we studied the altered capacities of the macrophages and lymphocytes to produce cytokines in conjunction with resistance to Listeria monocytegenes (LM) infection in mice Materials and Methods : BALB/c mice and Listeria monocytogenes were used. The mice were infected intraperitoneally with $10^5LM$ at 1 day after irradiation (300cGy) and sacrificed at 1, 3, 5 days after infection, and then the numbers of viable LM per spleen in the irradiated and control group were counted. Tumor necrosis factor-alpha ($TNF-\alpha$), interferon-gamma ($IFN-\gamma$). interleukin-2 (IL-2), and nitric oxide (NO) were assessed after irradiation. Results : Under gamma-ray irradiation with a dose range of 100-850cGy, the number of total splenocytes decreased markedly in a dose-dependent manner, while peritoneal macrophages did so slightly Cultured peritoneal macrophages produced more $TNF-\alpha$ in the presence of lipopolysaccharide (LPS) during the 24 hours after in vitro irradiation, but their capacity of $TNF-\alpha$ Production showed a decreased tendency at 5 days after in vivo total body irradiation. With 100cGy and 300cGy irradiation, cultured peritoneal macrophages produced more NO in the presence of LPS during the 24 hours after in vitro irradiation than without irradiation. Activated splenocytes from irradiated mice (300cGy) exhibited a decreased capacity to Produce IL-2 and $IFN-\gamma$ with Concavalin-A stimulation at 3 days after irradiation. When BALB/c mice were irradiated to the total body with a dose of 300cGy, they showed enhanced resistance during early innate phase, but a significant inhibition of resistance to LM was found in the late innate and acquired T-cell dependent phases. Conclusion : These results su99es1 that increased early innate and decreased late innate and acquired immunity to LM infection by ionizing radiation (300cGy) may be related to the biphasic altered capacity of the macrophages to produce $TNF-\alpha$ and the decreased capacities of the lymphocytes to produce IL-2 and $IFN-\gamma$ in addition to a marked decrease in the total number of cells.

• The Korean Journal of Food And Nutrition
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• v.26 no.4
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• pp.806-813
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• 2013

Agrimonia pilosa Ledeb. is a medicinal plant with anti-tumor, anti-oxidant, anti-inflammatory and anti-hyperglycemic activities. However, few studies of the anti-diabetic effect of A. pilosa on insulin resistance status have been performed. In the present study, the anti-diabetic effect of A. pilosa water extract (AP) was determined by investigating its ${\alpha}$-glucosidase inhibitory property, glucose utilization, and uptake, as well as insulin resistance mechanism of action in C2C12 skeletal muscle cells. Compared to positive control (acarbose), AP ($10mg/m{\ell}$) showed a similar ${\alpha}$-glucosidase inhibitory capacity. Glucose uptake was significantly increased by $1{\mu}m$ insulin treatment (p<0.05). However, palmitic acid (FFA, 1 mM) induced muscle insulin resistance and glucose uptake dysfunction. On the other hand, AP ($10{\mu}g/m{\ell}$) was capable of reversing the FFA-induced insulin resistance in C2C12 myotubes. Compared to control, AP ($100{\mu}g/m{\ell}$ without insulin) significantly increased the utilization of glucose (p<0.05) in C2Cl2 myotubes cultured in normal glucose (7 mM). AP treatment significantly increased the relative mRNA and protein expression levels of Akt. In particular, the effect of A. pilosa on the insulin signaling system is associated with the up-regulation of Akt genes and glucose uptake in C2Cl2 myotubes. These results suggest that A. pilosa is useful in the prevention of diabetes and the treatment of hyperglycemic disorders.

• Journal of Korean Ophthalmic Optics Society
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• v.7 no.1
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• pp.39-43
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• 2002

This study was investigated the anti-angiogenic activities of Cnidium officinale Makino and Tabanus bovinus by using Chorioallantoic membrane (CAM) and rat cornea. First experiment, the fertilized chicken eggs were kept in a humidified egg incubator at $37^{\circ}C$. After 4 days incubation, about 3 ml of albumin was aspirated from eggs with an hypodermic needles through a small hole drilled at the narrow end of the eggs, and the shell membrane on the floor of the air sac was peeled away. Embryos with chorioallantois of 3~5 mm in diameter were employed for the assay of antiangiogenic activity. Retinoic acid was used as a positive control for this experiment. After 48 h of treatment. branching pattern of blood vessels below coverslip containing retinoic acid ($10{\mu}g/egg$) was dramatically decreased. A simiar angiogenic inhibition was observed in the CAM treated with $50{\mu}g/egg$ of Cnidium omcinale Makino and Tabanus bovinus extracts. Second experiment, rat corneal neovascularization was induced by suturing (one stitch) the cornea with 10-0 nylon, and terramycin was applied on the cornea for I week to prevent corneal inflammation. In the cornea of rats untreated with herbal extracts, numerous vessels were usually seen invading the cornea by day 2 or 3 after suture, and reaching the lesion area within 5~6 days. Corneal neovascularization was gradually increased and peaked at 3 weeks. In contrast to this, herbal extracts conspicuously inhibited the angiogenesis, Oral administration of herbal extracts (20 mg/kg body weight/day) for 4 weeks significantly inhibited the rat corneal angiogenesis induced by suture, and the length of blood vessels in herbal medicine-treated rat cornea was conspicuously lower than that in control animals. A similar phenomenon was also observed in the rat cornea treated with thalidomide (200 mg/kg body weight/day). These findings indicate the anti-angiogenic properties of Cnidium officinale Makino and Tabanus bovinus, suggesting that these properties may be one of the pharmacological mechanisms underlying the anti-tumor and anti-metastatic activities of herbal extracts tested in this study.

• Journal of Life Science
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• v.15 no.2 s.69
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• pp.169-175
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• 2005

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a phytoalexin found in grape skins, peanuts, and red wine, has been reported to have a wide range of biological and pharmacological properties. $Amyloid-\beta$ deposition and senile plaque-associated astrocytes are common neuropathological features of Alzheimer's disease. In this study, we have explored the effects of resveratrol on $amyloid-\beta-peptide-mediated$ cytotoxicity in vitro and modulation of cell growth-regulatory gene products in astroglioma C6 cells to elucidate its possible mechanism for anti-cytotoxicity. Exposure of C6 cells to $Amyloid-\beta$ resulted in dose-dependent growth inhibition and morphological changes of C6 cells, which were recovered by pre-treatment with resveratrol. The anti-proliferative effect of $amyloid-\beta$ was associated with the induction of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21 (WAF1/CIP1) expression assessed by RT-PCR and Western blot analysis in time-dependent manner in C6 cells. In addition, the pro-apoptotic Bax expression was also up-regulated in $amyloid-\beta-treated$ C6 cells without alteration of anti-apoptotic Bcl-2 and $Bcl-X_L$ expression. However, pre-treatment of resveratrol significantly inhibited $amyloid-\beta-induced$ p53, p21 and Bax levels, suggesting that the modulation of p53, p21 and Bax levels could be one of the possible pathways by which resveratrol functions as anti-cytotoxic agent. Our results demonstrate that resveratrol may enhance the protection against $amyloid-\beta-induced$ cytotoxicity by promoting the survival of glial cells.