• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.2
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• pp.194-201
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• 2016

The anti-inflammatory activity of ethanol extract from Chondrus nipponicus Yendo (CNYEE) was investigated by measuring production of a lipopolysaccharide-induced inflammatory response mediator. CNYEE had no cytotoxic effects on proliferation of macrophages compared to the control. CNYEE significantly inhibited (over 50%) NO production at $50{\mu}g/mL$, with inhibitory effects on expression levels of cytokines such as interleukin (IL)-6, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and IL-$1{\beta}$. In particular, IL-6 inhibitory activity of CNYEE was higher than 70% at $100{\mu}g/mL$. CNYEE also reduced protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor (NF)-${\kappa}B$ in a dose-dependent manner. CNYEE also significantly reduced phosphorylation of p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase. Therefore, these results suggest that CNYEE may have anti-inflammatory effects by modulating the NF-${\kappa}B$ and mitogen-activated protein kinases signaling pathways and may be used as an anti-inflammatory therapeutic material.

• YAKHAK HOEJI
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• v.46 no.6
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• pp.426-432
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• 2002

Cervical cancer is one of the leading causes of female death from cancer worldwide with about 500,000 deaths per year. A strong association between certain human papilloma viruses (HPV type 16 and 18) and cervical cancer has been well known. An extract of Saururus chinensis, named as PE-46, has been used to investigate whether this agent has the ability of inhibiting the oncogenes E6 and E7 of HPV type 16. PE-46 inhibited the proliferation of human cervical cancer cell lines in a dose response manner. PE-46 also inhibited the in vitro binding of E6 and E6AP which are essential for the binding and degradation of the tumor suppressor p53. In addition, PE-46 inhibited the in vitro binding of E7 and Rb which is essential tumor suppressor for the control of cell cycle. The levels of mRNA for E6 and E7 were also decreased by PE-46. SiHa cells treated with PE-46 induced G0/G1 arrest, resulting in inhibition of growth. Our study showed that the PE-46 can inhibit the cervical carcinomas via both inhibition of bindings between oncogenes and tumor suppressors, and inhibition of G1longrightarrowS transition. PE-46 inhibited the oncogenecity of E6 and E7 of HPV 16 type, thus could be used as a putative modulating agent for the treatment of cervical carcinomas caused by HPV.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.231-238
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• 2005

Neuronal apoptotic events, which result in cell death, are occurred in hypoxic/ischemic conditions. Estradiol is a female sex hormone with steroid structure known to provide neuroprotection through multiple mechanisms in the central nervous system. This study was aimed to investigate the signal transduction pathway of $CoCl_2$-induced neuronal cell death and the inhibitory effects of estradiol. Administration of $CoCl_2$ decreased cell viability in both a dose- and time-dependent manner in PC12 cells. $CoCl_2$-induced cell death produced genomic DNA fragmentation and morphologic changes such as cell shrinkage and condensed nuclei. It was found that $CoCl_2$-treated cells increased the reactive oxygen species (ROS) as well as caspase-8, -9 and -3 activities. However, pretreatment with estradiol before exposure to $CoCl_2$ prevented the reduction in cell viability reduction and attenuated DNA fragmentation and morphologic changes caused by $CoCl_2$. Furthermore, the $CoCl_2$-induced increases of ROS levels and caspases activities were attenuated by estradiol. Gene expression analysis revealed that estradiol blocked the underexpression of the Bcl-2 and ameliorated the increase in the release of cytochrome c from mitochondria into cytoplasm and Fas-ligand (Fas-L) upregulated by $CoCl_2$. These results suggest that $CoCl_2$ induce apoptosis in PC12 cells through both mitochondria- and death receptor-mediated cell death pathway. Estradiol was found to have a neuroprotective effect against $CoCl_2$-induced apoptosis through the inhibition of ROS production and by modulating apoptotic effectors associated with the mitochondria- and death-dependent pathway in PC12 cells.

• Korean Journal of Head & Neck Oncology
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• v.18 no.2
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• pp.150-156
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• 2002

Objectives: Most of human cancers may result from exposure to environmental carcinogens, and individual effectiveness in the detoxification of these chemicals will influence susceptibility to malignant disease. Glutathione S-Transferases(GSTs) enzymes are involved in the detoxification of active metabolites of many carcinogens from tobacco smoke and may be important in modulating susceptibility to smoke-related cancer. The purpose of this study is to determine the polymorphism of GSTM1, GSTT1, and GSTP1 in control group and head and neck squamous cell carcinoma group of Korean, and to investigate the effect of GSTs polymorphism on the risk of head and neck cancer. Materials and Methods: A hospital-based case-control study was performed with a group of 133 control individual and 136 head and neck squamous cell carcinoma patients. The polymorphisms of GSTs were analysed using polymerase chain reaction in GSTM1 and GSTTl, and polymerase chain reaction-restriction fragment length polymorphism in GSTP1. Results: The relative risk (odds ratio) of GSTM(-) genotype was 1.14(95% CI, 0.70-1.85) compared to GSTM1(+). The odds ratio of GSTTl(-) genotype was 0.91(95% CI, 0.55-1.50). In old age($65$) group, the odds ratio of GSTT1(-) genotype was 5.2(95% CI, 1.53-17.89). The GSTP1 Val/Val genotype conferred a 1.7-fold risk(95% CI, 0.40-7.34) of head and neck cancer compared with GSTP1 Ile/Ile genotype. Among the combined genotypes of GSTs, GSTM1(-)/GSTT1(+)/GSTP1 Val/Val and GSTM1(-)/GSTTl(-)/GSTP1 Ile/Val genotypes conferred a 2.6-fold and 1.3-fold risk(95% CI, 0.24-14.15 and 0.43-3.14) compared with the GSTM1(+)/GSTTl(+)/GSTP1 Ile/Ile genotype, respectively. Conclusion: Polymorphism of GSTs might modulate susceptibility to head and neck cancer in Korean population. The genotype of GSTP1 Val/Val and combined genotypes of GSTM1(-)/GSTT1(+)/GSTP1 Val/Val, and GSTM1(-)/GSTT1(-)/GSTP1 Ile/Val might be important risk factors to determine the individual susceptibility to head and neck squamous cell carcinoma.

• Korean Journal of Food Science and Technology
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• v.50 no.4
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• pp.444-450
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• 2018

Dendritic cells (DCs) are potent antigen-presenting cells that play a pivotal role in modulating both innate and adaptive immunity. This study examined the immunomodulatory activities of hot-water extracts of bee pollen (BPW) in bone-marrow derived DCs (BMDC) and mice splenocytes. BMDCs isolated from mice were treated with 250 and $500{\mu}g/mL$ BPW for 24 h. BPW, up to $500{\mu}g/mL$, did not display any cellular toxicity against BMDCs. In fact, it functionally induced BMDC activation via augmentation of CD80, CD86, and major histocompatibility complex (MHC) class I/II expression and pro-inflammatory cytokine (tumor necrosis factor; $TNF-{\alpha}$, interleukin; IL-6, and $IL-1{\beta}$) production. Interestingly, BPW treatment significantly increased the production of interferon $(IFN)-{\gamma}$ in splenocytes, suggesting its possible contribution to Th1 polarization in immune response. Taken together, these findings suggest that BPW may regulate innate and adaptive immunity via DC activation and Th1 polarization in immune responses.

• Journal of Life Science
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• v.24 no.2
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• pp.196-208
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• 2014

During the life cycle of plants, water deficit leads to an adverse effect on its growth and development. To increase the productivity of crops, overcoming such drought stress is one of the most important issues in the field of plant study. Among plant hormones, the phytohormone, abscisic acid (ABA) plays a crucial role in eliciting resistance to drought stress as well as in multiple developmental processes, such as seed germination, stomatal closure, and seedling growth. Therefore, further understanding of the ABA-mediated signal transduction pathway in plants is an effective strategy to generate drought-tolerant plants. Posttranslational modification, such as phosphorylation and ubiquitination, is an efficient mechanism for plants to acquire quick adaptation against environmental stress conditions since this process directly affects pre-existing signaling components by modulating protein activity and stability. Here, recent reports on ABA signaling are reviewed, especially focusing on ABA transport, perception, signaling, and posttranslational modification in ABA-mediated cellular responses. Also, we present future prospects on how the control of such a mechanism can be applied to generate useful agricultural crops.

• Toxicological Research
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• v.34 no.4
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• pp.325-332
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• 2018

The mechanism of the previously reported antidiabetic effect of Basella alba is unknown. This study investigated the role of B. alba aqueous leaf extract in the modulation of inflammatory cytokines and islet morphology in streptozotocin-induced diabetic rats. Forty male Wistar rats, between 8 and 10 weeks old, were randomly divided into four groups (n = 10) and administered the following treatments: Healthy control (H-c) and Diabetic control (D-c) animals received normal saline 0.5 mL/100 g body weight daily, while Healthy Treatment (H-Ba) and Diabetic Treatment (D-Ba) rats received the plant extract 200 mg/kg body weight daily. All treatments were administered by oral gavage. Diabetes was induced in D-c and D-Ba rats by a single intraperitoneal injection of streptozotocin (55 mg/kg body). The body weight and fasting blood sugar (FBS) levels were recorded every week for 4 weeks, after which the rats were euthanized and samples collected for further analysis. After the experiment, FBS level was significantly reduced (p < 0.0001) in rats in the D-Ba group, but increased (p < 0.001) in rats in the D-c group. The absolute (H-c and H-Ba vs D-c, p < 0.05) and relative (D-Ba vs H-c, p < 0.05; D-Ba vs H-Ba, p < 0.005) weights of the pancreases were significantly higher after the experiment. The rats in the D-c group had significantly higher levels of serum interleukin-$1{\beta}$ (p < 0.001 vs H-c; p < 0.05 vs H-Ba and D-Ba) and monocyte chemotactic protein-1 (p < 0.0001), but lower levels of interleukin-10 (p < 0.05) in comparison with the other groups. Histopathological examination revealed severe interstitial congestion, reduced islet area (p < 0.0001), and increased islet cell density in the D-c group compared with those in the D-Ba group. From these findings, it was concluded that the aqueous extract of B. alba stimulates the recovery of beta-islet morphology in streptozotocininduced diabetic rats by modulating the peripheral production of inflammatory cytokines.

• Korean Journal of Medicinal Crop Science
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• v.12 no.4
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• pp.304-308
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• 2004

Immune enhancing activities of water and ethanol extracts of Hypericum perforatum L. (HP) were examined. HP extracts inhibited the growth of human hepatocarcinoma, human gastric cancer cell and human breast cancer cells in concentration-dependent mammers over a concentration range of $0.05{\sim}1.0\;mg/ml$, showing inhibiton of more than 80% with the concentration of 1.0 mg/ml. However, HP the same concentration. Overall selectivity of the extracts on the three human cancer lines was over 3.5, which is higher than those from the conventional herbs. The growth of human immune B and T cells was enhanced up to 1.4 to 2.0 folds by the addition of the extracts for 4 days, compared to controls. Ethanol extracts of HP after 6 days incubation increased the secretions of tumor necrosis factor-alpha $(TNF-{\alpha})$ from T cells and interleukin-6 (IL-6) from B cells to 6.7 pg/cell and 6.8 pg/cell, respectively. These results suggest that HP has a potent immune enhancing effect.

• Microbiology and Biotechnology Letters
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• v.44 no.3
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• pp.383-390
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• 2016

Mesenchymal stem cells (MSCs) are multipotent stem cells that can be differentiated into a variety of cell types, including adipocytes, osteoblasts, chondrocytes, β-pancreatic islet cells, and neuronal cells. MSCs have been reported to exhibit immunomodulatory effects in many diseases. Many studies have reported that MSCs have distinct roles in modulating inflammatory and immune responses by releasing bioactive molecules. Exosomes are cell-derived vesicles present in biological fluids, including the blood, urine, and cultured medium of cell cultures. In this study, we investigated the immunomodulatory effects of mouse adipose tissue-derived MSCs (mAD-MSCs), cultured medium (MSC-CM) of mAD-MSCs, and mAD-MSC-derived exosomes (MSC-Exo) on lipopolysaccharide (LPS)-induced RAW 264.7 cells. We observed that the expression levels of IL-1β, TNF-α, and IL-10 were significantly increased in LPS-stimulated RAW 264.7 cells compared to those in LPS-unstimulated RAW 264.7 cells. Additionally, these values were significantly (p < 0.05) decreased in mAD-MSCs-RAW 264.7 cell co-culture groups, MSC-CM-treated groups, and MSC-Exo-treated groups. MSCs can modulate the immune system in part by secreting cytokines and growth factors. We observed that immunomodulatory factors such as IL-1β, TNF-α, and IL-10 were secreted by mAD-MSCs under co-culturing conditions of mAD-MSCs with activated RAW 264.7 cells. In addition, mAD-MSC-derived exosomes exhibited similar immunomodulatory effects in activated RAW 264.7 cells. Therefore, our results suggest that mAD-MSCs have an immunomodulatory function through indirect contact.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.661-670
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• 2018

Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor $(TNF)-{\alpha}$, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of $TNF-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.