The effect of nitric oxide (NO) on antioxidant system and protective mechanism against oxidative stress under UV-B radiation was investigated in leaves of maize (Zea mays L.) seedlings during 3 days growth period. UV-B irradiation caused a decrease of leaf biomass including leaf length, width and weight during growth. Application of NO donor, sodium nitroprusside (SNP), significantly alleviated UV-B stress induced growth suppression. NO donor permitted the survival of more green leaf tissue preventing chlorophyll content reduction and of higher quantum yield for photosystem II than in non-treated controls under UV-B stress, suggesting that NO has protective effect on chloroplast membrane in maize leaves. Flavonoids and anthocyanin, UV-B absorbing compounds, were significantly accumulated in the maize leaves upon UV-B exposure. Moreover, the increase of these compounds was intensified in the NO treated seedlings. UV-B treatment resulted in lipid peroxidation and induced accumulation of hydrogen peroxide ($H_2O_2$) in maize leaves, while NO donor prevented UV-B induced increase in the contents of malondialdehyde (MDA) and $H_2O_2$. These results demonstrate that NO serves as antioxidant agent able to scavenge $H_2O_2$ to protect plant cells from oxidative damage. The activities of two antioxidant enzymes that scavenge reactive oxygen species, catalase (CAT) and ascorbate peroxidase (APX) in maize leaves in the presence of NO donor under UV-B stress were higher than those under UV-B stress alone. Application of 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3- oxide (PTIO), a specific NO scavenger, to the maize leaves arrested NO donor mediated protective effect on leaf growth, photosynthetic pigment and free radical scavenging activity. However, PTIO had little effect on maize leaves under UV-B stress compared with that of UV-B stress alone. $N^{\omega}$-nitro-L-arginine (LNNA), an inhibitor of nitric oxide synthase (NOS), significantly increased $H_2O_2$ and MDA accumulation and decreased antioxidant enzyme activities in maize leaves under UV-B stress. This demonstrates that NOS inhibitor LNNA has opposite effects on oxidative resistance. From these results it is suggested that NO might act as a signal in activating active oxygen scavenging system that protects plants from oxidative stress induced by UV-B radiation and thus confer UV-B tolerance.
Sanguinarine is a benzophenanthridine alkaloid originally isolated from the roots of Sanguinaria canadensis. It has multiple biological activities (e.g., antioxidant and antiproliferative) and immune-enhancing potential. In this study, we explored the proapoptotic properties and modes of action of sanguinarine in human hepatocellular carcinoma HepG2 cells. Our results revealed that sanguinarine inhibited HepG2 cell growth and induced apoptosis in a dose-dependent manner. The induction of apoptosis by sanguinarine was associated with the up-regulation of Fas and Bax, the release of cytochrome c from the mitochondria to the cytosol, and the loss of the mitochondrial membrane potential. In addition, sanguinarine activated caspase-9 and -8, initiator caspases of the intrinsic and death extrinsic pathways, respectively, and caspase-3, accompanied by proteolytic degradation of poly (ADP-ribose) polymerase. Sanguinarine also triggered the generation of reactive oxygen species (ROS). The elimination of ROS by N-acetylcysteine reversed sanguinarine-induced apoptosis. Furthermore, sanguinarine induced the dephosphorylation of Akt and the phosphorylation of mitogen-activated protein kinases, including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38. The growth inhibition was enhanced by the combined treatment of sanguinarine with a phosphatidylinositol 3'-kinase (PI3K) inhibitor and an ERK inhibitor but not JNK and p38 inhibitors. Overall, our data indicate that the proapoptotic effects of sanguinarine in HepG2 cells depend on ROS production and the activation of both intrinsic and extrinsic signaling pathways, which is mediated by blocking PI3K/Akt and activating the ERK pathway. Thus, our data suggest that sanguinarine may be a natural compound with potential for use as an antitumor agent in liver cancer.
Kwon Hong Rho;Ko Eun Jung;Bae Hyun Su;Hong Moo Chang;Jung Seung Gi;Shin Min Kyu
Journal of Physiology & Pathology in Korean Medicine
/
v.18
no.4
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pp.1021-1027
/
2004
Panax ginseng has been used as a typical tonic medicine in Asian countries, such as Korea, China, and Japan. It has been reported that ginsenoside Rg1 in Panax ginseng increases the proportion of T helper cells in the whole T cells and promotes IL-2 gene expression in murine splenocytes. These studies imply that ginsenoside Rg1 increases the immune activity of CD4+ T cell, however the exact mechanism of ginsenoside Rg1 on helper T cell remains to be verified. The present study tried to elucidate the direct effect of Rg1 on helper T cell s activities and its Th1/Th2 lineage development. The results demonstrated that ginsenoside Rg1 had not mitogenic effects on the unstimulated CD4+ T cell, but augmented CD4+ T cell proliferation upon activating with anti-CD3/anti-CD28 antibodies in a dose dependent manner. Rg1 also enhanced the expression of cell surface protein CD69 on CD4+ T cell. In Th0 condition, ginsenoside Rg1 increases the expression of IL-2 mRNA, and enhances the expression of IL-4 mRNA on CD4+ T cells, suggesting Rg1 prefer to induce Th2 lineage development. In addition, ginsenoside Rg1 increases IL-4 secreting CD4+ T cell under Th2 skewed condition, while decreases IFN-γ secreting cell in Th1 polarizing condition. Thus, Rg1 enhances Th2 lineage development from naive CD4+ T cell both by increasing Th2 specific cytokine secretion and by repressing Th1 specific cytokine production. Therefore, these results suggest that ginsenoside Rg1 might be desirable agent for enhancing CD4+ T cell's activity, as well as the correction of Th1 dominant pathological disorders.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
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v.27
no.4
/
pp.314-320
/
2001
Matrix metalloproteinases have long been viewed as ideal candidates for proteinases that enables tumor cells to permeated basement membrane defenses and invade surrounding tissue. There is growing evidence that the MMPs have an expanded role, as they are important for the creation and maintenance of a microenvironment that facilitates growth and angiogenesis of tumors at primary and metastatic sites. MT-MMPs are not secreted but instead remaining attached to cell surfaces. Although not all of the MT-MMPs are fully characterized, MT-MMPs have important role in localizing and activating secreted MMPs. The MMP genes are transcriptionally responsive to a wide variety of oncogene, growth factors, cytokine, and hormones. Currently, a number of MMP inhibitors are being developed and some have reached clinical trials as anti-metastatic or anti-cancer therapies. MT1-MMP is involved in the activation of proMMP-2. MT1-MMP is significant not only as a tumor marker but as a new target for chemotherapy against cancer. The purpose of this study was to evaluate the effects of protein kinase C inhibitor(genistein) on the proliferation of HT1080 and expression of MT1-MMP mRNA. Human fibrosarcoma cell line HT1080 was cultured and divided 2 groups. The experimental group was treated with $100{\mu}M$ genistein and incubated 12h, 24h for $[3^H]-thymidine$ uptake assay and northern hybridization individually. And the control group was treated with same amount of PBS for the above procedures. $[3^H]-thymidine$ incorporation was measured with ${\beta}$ ray detector. And RT-PCR and northern blotting for MT1-MMP mRNA was performed. The results were as follows 1. $[3^H]-thymidine$ uptake was reduced in experimental group with statistical significance. 2. MT1-MMP mRNA expression was significantly reduced in experimental group. These results showed that protein kinase C inhibitor (genistein) inhibited proliferation of HT1080 and almost completely blocked transcription of MT1-MMP mRNA. So, it is possible to use the protein kinase inhibitor (genistein) as anti-metastatic and anti-proliferative agent.
Journal of Korean Society of Environmental Engineers
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v.30
no.9
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pp.900-906
/
2008
It was studied to utilize wasted food as a starting material to produce for activated carbon. The wasted food was chemically activated with zinc chloride. Experiments were carried out at different chemical ratios(activating agent/wasted foods), activation temperatures, and activation time. The activated products were characterized by measuring the iodine and methylene blue number, the BET surface area, the pore volume, the micropore ratio, the pore diameter, the yields and the scanning electron microscope(SEM). For the products activated by impregnation ratio of 1.0 of ZnCl$_2$ at 500$^{\circ}C$ for 60 min in a rotary kiln reactor had iodine number of 480 mg/g, methylene blue number of 95 mL/g, BET surface area of 410 m$^2$/g, pore volume of 0.248 cm$^3$/g, and average pore diameter of 2.43 nm, respectively. The activated carbon obtained had the contribution of micropore area of 70.7% to the total pore area and micropore volume of 53.2% to the total pore volume.
Objectives : Oxidative stress due to excessive accumulation of reactive oxygen species (ROS) is one of the risk factors for the development of several chronic diseases, including neurodegenerative diseases. Methods : In the present study, we investigated the protective effects of cheongnoemyeongsin-hwan (CNMSH) against oxidative stress‑induced cellular damage and elucidated the underlying mechanisms in neuronal-derived SH-SY5Y cells. Results : Our results revealed that treatment with CNMSH prior to hydrogen peroxide (H2O2) exposure significantly increased the SH-SY5Y cell viability, indicating that the exposure of the SH-SY5Y cells to CNMSH conferred a protective effect against oxidative stress. CNMSH also effectively attenuated H2O2‑induced comet tail formation, and decreased the phosphorylation levels of the histone ${\gamma}H2AX$, as well as the number of apoptotic bodies and Annexin V‑positive cells. In addition, CNMSH exhibited scavenging activity against intracellular ROS generation and restored the mitochondria membrane potential (MMP) loss that were induced by H2O2, suggesting that CNMSH prevents H2O2‑induced DNA damage and cell apoptosis. Moreover, H2O2 enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)-polymerase, a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with CNMSH. Furthermore, CNMSH increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear factor-erythroid 2-related factor 2 (Nrf2). According to our data, CNMSH is able to protect SH-SY5Y cells from H2O2-induced apoptosis throughout blocking cellular damage related to oxidative stress through a mechanism that would affect ROS elimination and activating Nrf2/HO-1 signaling pathway. Conclusions : Therefore, we believed that CNMSH may potentially serve as an agent for the treatment and prevention of neurodegenerative diseases caused by oxidative stress.
In this work, mesoporous carbons (CMK-3) were prepared by a conventional templating method using mesoporous silica (SBA-15) for using catalyst supports in polymer electrolyte membrane fuel cells (PEMFCs). The CMK-3 were chemically activated to obtain high surface area and small pore diameter with different potassium hydroxide (KOH) amounts, i.e., 0, 1, 3, and 4 g as an activating agent. And then Pt-Ru was deposited onto activated CMK-3 (K-CMK-3) by a chemical reduction method. The characteristics of Pt-Ru catalysts deposited onto K-CMK-3 were determined by surface area and pore size analysis, X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), and inductive coupled plasma-mass spectrometry (ICP-MS). The electrochemical properties of Pt-Ru/K-CMK-3 catalysts were also analyzed by cyclic voltammetry (CV). From the results, the K3g-CMK-3 carbon supports activated with 3 g KOH showed the highest specific surface areas. In addition, the K3g-CMK-3 led to uniform dispersion of Pt-Ru onto K-CMK-3, resulted in the enhancement of elelctro-catalystic activity of Pt-Ru catalysts.
Little is known about the cardiovascular effects of Lycopene, an anti-cancer and anti-oxidative agent. In this study, we executed a series of experiments with vascular endothelial cells to disclose the cardiovascular functions of lycopene. From our in vitro experiments, lycopene was determined to act as a stimulant to induce endothelial cell proliferation and migration. In addition, lycopene was shown to inhibit lipopolysaccharide (LPS)-induced adhesion of THP-1 leukocytes to endothelial cells, as well as activating mitogen activated protein kinase (MAPK) family members, ERK, JNK and p38 MAPK. Both ERK and p38 MAPK were involved in lycopene-induced cell proliferation, while JNK was involved in lycopene-dependent cell migration. Taken together, lycopene activates MAPK family members which regulate cell proliferation and migration. Lycopene differentially blocks LPS-dependent adhesion for THP-1 to endothelial cells, indicating that lycopene is likely to regulate a variety of vascular functions.
Park, Sora;Thomas, Shalom Sara;Cha, Youn-Soo;Kim, Kyung-Ah
Journal of Nutrition and Health
/
v.53
no.6
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pp.583-595
/
2020
Purpose: This study examined the effects of Sargassum horneri extracts on palmitic acid (PA)-induced endoplasmic reticulum (ER) stress in HepG2 cells. Methods: HepG2 cells were treated with varying concentrations of S. horneri extract or PA, and the cell viability was measured by water soluble tetrazolium salts analysis. The effective induction of ER stress and the effects of S. horneri were investigated through an examination of the ER stress-related genes, such as activating transcription factor 4 (ATF4), X-box binding protein (XBP1s), C/EBP homologous protein (CHOP), and 78-kDa glucose-regulated protein (GRP78) by quantitative reverse transcription polymerase chain reaction. The expression and activation levels of unfolded protein response (UPR) associated proteins, such as inositol-requiring enzyme-1α (IRE1α), eukaryotic translation initiation factor 2 alpha submit (eIF2α), and CHOP were examined by western blot analysis. Results: The treatment with PA increased the expression of UPR associated genes significantly and induced ER stress in a 12-hour treatment. Subsequent treatment with S. horneri reduced mRNA expression of ATF4, GRP78, and XBP1s. In addition, the protein levels of phosphate (p)-IRE1α, p-elF2α, and CHOP were also reduced by a treatment with S. horneri. An analysis of sirtuin (SIRT) mRNA expression in the S. horneri and PA-treated HepG2 cells showed that S. horneri increased the levels of SIRT2, SIRT6, and SIRT7, which indicates a possible role in reducing the expression of ER stress-related genes. Conclusion: These data indicate that S. horneri can exert an inhibitory effect on ER stress caused by PA and highlight its potential as an agent for managing various ER stress-related diseases.
In this study, we investigated the adsorption characteristics of methyl orange (MO), an anionic dye, on ginkgo shell-based activated carbon (AC). For this purpose, ACs (GS-1, GS-2, and GS-4) with different textural properties were prepared using ginkgo shells and potassium hydroxide (KOH), a representative chemical activating agent. The correlation between the textural characteristics of AC prepared and the mixing ratio of KOH was investigated using nitrogen adsorption/desorption isotherms. The MO adsorption equilibrium experiment on the prepared ACs was conducted under different pH (pH 3~11) and temperature (298~318 K) conditions, and the results were investigated by Langmuir, Freundlich, Sips and temperature-dependent Sips equations. The feasibility of the MO adsorption treatment process of the prepared AC was also investigated using the dimensionless Langmuir separation factor. The heterogeneous adsorption properties of MO for the prepared AC examined using the adsorption energy distribution function (AED) were closely related to the system temperature and textural characteristics of AC. The kinetic results of the batch adsorption performed at different temperatures can be satisfactorily explained by the homogeneous surface diffusion model (HSDM), which takes into account the external mass transfer, intraparticle diffusion, and active site adsorption. The relationship between the activation energy value obtained by the Arrhenius plot and the adsorption energy distribution function value was also investigated. In addition, the adsorption process mechanism of MO on the prepared AC was evaluated using Biot number.
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