• Korean Chemical Engineering Research
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• v.45 no.3
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• pp.269-276
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• 2007

$TiO_2$-containing pitch fibers were prepared and various stabilization variables were investigated by characterizations of the fibers and behaviors of $TiO_2$ particles in the optimum stabilization conditions. When pitch fiber was stabilized by air at the optimum condition, the fiber weight increased as an increase of the stabilization temperature and a decrease of $TiO_2$ concentration. The carbonization yield was 71~82 wt.%, showing a decrease of the yield with the $TiO_2$ increase caused by the catalytic activity of $TiO_2$ to combustion. During the stabilization, newly developed carbonyl and carboxyl groups were introduced on the fiber surface and cross-linking reactions were progressed resulting the thermosetting property, which was verified by the replacement of hydrogen with oxygen. Pore size of the activated carbon fiber was increased by an increase in $TiO_2$ concentration. In the considerations of the aggregation behaviors of the $TiO_2$ particles, the optimum stabilization conditions of 0.5 wt.% $TiO_2$ containing petroleum-based pitch fiber were suggested as $280^{\circ}C$, 3 hr.

• 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.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.443-455
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• 2020

The thioredoxin (Trx) system plays critical roles in regulating intracellular redox levels and defending organisms against oxidative stress. Recent studies indicated that Trx reductase (TrxR) was overexpressed in various types of human cancer cells indicating that the Trx-TrxR system may be a potential target for anti-cancer drug development. This study investigated the synergistic effect of auranofin, a TrxR-specific inhibitor, on sulforaphane-mediated apoptotic cell death using Hep3B cells. The results showed that sulforaphane significantly enhanced auranofin-induced apoptosis by inhibiting TrxR activity and cell proliferation compared to either single treatment. The synergistic effect of sulforaphane and auranofin on apoptosis was evidenced by an increased annexin-V-positive cells and Sub-G1 cells. The induction of apoptosis by the combined treatment caused the loss of mitochondrial membrane potential (ΔΨm) and upregulation of Bax. In addition, the proteolytic activities of caspases (-3, -8, and -9) and the degradation of poly (ADP-ribose) polymerase, a substrate protein of activated caspase-3, were also higher in the combined treatment. Moreover, combined treatment induced excessive generation of reactive oxygen species (ROS). However, treatment with N-acetyl-L-cysteine, a ROS scavenger, reduced combined treatment-induced ROS production and apoptosis. Thereby, these results deduce that ROS played a pivotal role in apoptosis induced by auranofin and sulforaphane. Furthermore, apoptosis induced by auranofin and sulforaphane was significantly increased through inhibition of the phosphoinositide 3-kinase (PI3K)/Akt pathway. Taken together, the present study demonstrated that down-regulation of TrxR activity contributed to the synergistic effect of auranofin and sulforaphane on apoptosis through ROS production and inhibition of PI3K/Akt signaling pathway.

• Journal of Life Science
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• v.23 no.11
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• pp.1342-1350
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• 2013

We examined the effect of hydrogen sulfide ($H_2S$) in chemical hypoxia-induced injury in mouse hepatocytes. Cell viability was significantly decreased by cobalt chloride ($CoCl_2$), a well-known hypoxia mimetic agent in a time- and dose- dependent manner. Sodium hydrosulfide (NaHS, a donor of $H_2S$) pretreatment before exposure to $CoCl_2$ significantly attenuated the $CoCl_2$-induced decrease of cell viability. $CoCl_2$ treatment resulted in an increase of intracellular ROS generation, which is inhibited by NaHS or N-acetyl-cysteine (NAC, a ROS scavenger), and p38 MAPK phosphorylation, which is also blocked by NaHS or NAC. The $CoCl_2$-induced increase of the Bax/Bcl-2 ratio was attenuated by NaHS, NAC, and SB 203580 (p38 MAPK inhibitor). The $CoCl_2$-induced decrease of cell viability was also attenuated by NaHS, NAC, and SB 203580 pretreatment. Additionally, NaHS inhibited the $CoCl_2$-induced COX-2. Similar to the effect of NaHS, NAC blocked $CoCl_2$-induced COX-2 expression. Furthermore, NS-398 (a selective COX-2 inhibitor) attenuated not only the $CoCl_2$-induced increase of the Bax/Bcl-2 ratio, it also decreased cell viability. Taken together, $H_2S$ protects primary cultured mouse hepatocytes against $CoCl_2$-induced cell injury through inhibition of the ROS-activated p38 MAPK cascade and the COX-2 pathway.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.31 no.1
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• pp.109-113
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• 1998

The clay and yellow loess have capability to adsorb and precipitate particles. The removal efficiencyes of those flocculents on the dinoflagellate, Cochlodinium polykrikoides, have been studied in laboratory and in field near Tongyong fish farm in September, 1996. The removal efficiencyes in the laboratory experiment was $43\%$ for $2\;g/{\ell}$, $64\%$ for $6g/{\ell}$ and $88\%$ for $10\;g/{\ell}$ in one hour after dispersion. No big difference of removal efficiency was found between the raw and the acid-activated loess. In the field survey, the removal rates ranged from 72 to $80\%$ in 30 min after the dispersion. The effect of loess scattering on water quality was estimated. The concentrations of dissolved inorganic nitrogen (DIN), chemical of gen demand (COD) and chlorophyll a decreased more or less after dispersion, while the concentration of suspended solid (SS) increased. The concentrations of dissolved oxygen (DO) and dissolved inorganic phosphorous (DIP) were kept constant. These results indicated that the dispersion concentration of more than $10g/{\ell}$ has a good removal efficiency of above $80\%$ without big variation of water quality after dispersion of yellow loess.

• Asian-Australasian Journal of Animal Sciences
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• v.32 no.11
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• pp.1776-1788
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• 2019

Objective: The demands for measures to improve disease resistance and productivity of livestock are increasing, as most countries prohibit the addition of antibiotics to feed. This study therefore aimed to uncover functional feed additives to help enhance livestock immunity and disease resistance, using Acanthopanax sessiliflorus fruit extract (ASF). Methods: ASF was extracted with 70% EtOH, and total polyphenolic and catechin contents were measured by the Folin-Ciocalteu and vanillin assay, respectively. The 3D4/31 porcine macrophage cells ($M{\Phi}$) were activated by phorbol 12-myristate 13-acetate (PMA), and cell survival and growth rate were measured with or without ASF treatment. Flow-cytometric analysis determined the lysosomal activity, reactive oxygen species levels (ROS), and cell cycle distribution. Nuclear factor kappa B ($NF-{\kappa}B$) and superoxide dismutase (SOD) protein expression levels were quantified by western blotting and densitometry analysis. Quantitative polymerase chain reaction was applied to measure the lipid metabolism-related genes expression level. Lastly, the antibacterial activity of 3D4/31 $M{\Phi}$ cells was evaluated by the colony forming unit assay. Results: ASF upregulated the cell viability and growth rate of 3D4/31 $M{\Phi}$, with or without PMA activation. Moreover, lysosomal activity and intracellular ROS levels were increased after ASF exposure. In addition, the antioxidant enzyme SOD2 expression levels were proportionately increased with ROS levels. Both ASF and PMA treatment resulted in upregulation of $NF-{\kappa}B$ protein, tumor necrosis factor $(TNF){\alpha}$ mRNA expression levels, lipid synthesis, and fatty acid oxidation metabolism. Interestingly, co-treatment of ASF with PMA resulted in recovery of $NF-{\kappa}B$, $TNF{\alpha}$, and lipid metabolism levels. Finally, ASF pretreatment enhanced the in vitro bactericidal activity of 3D4/31 $M{\Phi}$ against Escherichia coli. Conclusion: This study provides a novel insight into the regulation of $NF-{\kappa}B$ activity and lipid metabolism in $M{\Phi}$, and we anticipate that ASF has the potential to be effective as a feed additive to enhance livestock immunity.

• Journal of Life Science
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• v.31 no.4
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• pp.400-409
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• 2021

Sanguinarine, a natural benzophenanthridine alkaloid, has been considered a potential therapeutic target for the treatment of cancer because it can induce apoptosis in human cancer cells; however, the underlying mechanisms of action still remain unclear. Tumor suppressor p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to anticancer agents. Therefore, in the present study, the role of p53 during apoptosis induced by sanguinarine was investigated in p53wild type (WT, p53+/+) and p53null (p53+/+) HCT116 colon carcinoma cells. Sanguinarine significantly caused greater reductions in cell viability in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells. Consistently, sanguinarine promoted more DNA damage and apoptosis in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells while increasing the expression of p53 and cyclin-dependent kinase inhibitor p21^WAF1/CIP1. Sanguinarine increased the activity of caspase-8 and caspase-9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and it activated caspase-3, a typical effect caspase, in HCT116 (p53+/+) cells. Sanguinarine also increased the generation of reactive oxygen species (ROS), and the Bax/Bcl-2 ratio, while destroying the integrity of mitochondria in HCT116 (p53+/+) cells, but not in HCT116 (p53-/-) cells. Overall, the results indicate that sanguinarine induced p53-dependent apoptosis through ROS-mediated activation of extrinsic and intrinsic apoptotic pathways in HCT116 colorectal cancer cells.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.04a
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• pp.113-113
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• 2019

Diallyl trisulfide (DATS) is an organic polysulfide compound found in garlic. Although certain studies have demonstrated that DATS possesses strong anti-inflammatory activity, the underlying molecular mechanisms remain largely unresolved. In this study, we examined whether DATS exerts anti-inflammatory activity and investigated the possible mechanisms. Our results indicated that DATS significantly suppressed the lipopolysaccharide (LPS)-induced release of nitric oxide (NO) and prostaglandin E2 by inhibiting inducible NO synthase and cyclooxygenase-2 expression at the transcriptional and post-transcriptional levels in RAW 264.7 macrophages. DATS also down-regulated Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 expression, and inhibited nuclear translocation of nuclear transcription factor-kappa B (NF-${\kappa}B$) in LPS-stimulated 264.7 macrophages. Furthermore, we found that these inhibitory effects of DATS were associated with the inhibition of chemokine receptor (CXCR4) and ligand (CXCL12) expression, and reactive oxygen species generation. Overall, the present data indicated that DATS had anti-inflammatory effects on LPS-activated macrophages, possibly via inhibiting the TLR4/NF-kB and/or chemokine signaling pathways, and DATS could be a potential drug therapy for inflammation and its associated diseases.

• Journal of Life Science
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• v.29 no.4
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• pp.436-441
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• 2019

Nelumbo nucifera, also known as sacred lotus, has mainly been used as a food throughout the Asian countries. In the present study, we prepared ethanol extracts from leaf (NL), seed (NS), and seedpod (NSP) of Nelumbo nucifera and investigated their anti-inflammatory activities in mouse macrophage RAW 264.7 cells. To evaluate the anti-inflammatory activities of NL, NS, and NSP, nitric oxide (NO) production was measured in LPS-stimulated RAW 264.7 cells. NL, NS, and NSP significantly reduced NO production in a dose-dependent manner without affecting cell viabilities. NL, NS, and NSP dramatically decreased the protein expression of pro-inflammatory genes such as iNOS and COX-2. NL, NS, and NSP also suppressed phosphorylation of MAPKs and the nuclear translocation of $NF-{\kappa}B$ p65 indicating they have their anti-inflammatory activities via regulating mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B ($NF-{\kappa}B$) pathways. In addition, we analyzed the production of reactive oxygen species (ROS) by the treatment of NL, NS, and NSP. All extracts reduced ROS production in a dose-dependent manner. And also, they increased heme oxygenase-1 (HO-1) protein expression and the nuclear translocation of nuclear respiratory factor 2 (Nrf2). In conclusion, our results suggest that Nelumbo nucifera has its anti-inflammatory activity via regulating MAPKs, $NF-{\kappa}B$, and Nrf2/HO-1 pathways.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.685-696
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• 2021

In this study, we investigated the inhibitory effect of 5-aminolevulinic acid (ALA), a heme precursor, on inflammatory and oxidative stress activated by lipopolysaccharide (LPS) in RAW 264.7 macrophages by estimating nitric oxide (NO), prostaglandin E2 (PGE2), cytokines, and reactive oxygen species (ROS). We also evaluated the molecular mechanisms through analysis of the expression of their regulatory genes, and further evaluated the anti-inflammatory and antioxidant efficacy of ALA against LPS in the zebrafish model. Our results indicated that ALA treatment significantly attenuated the LPS-induced release of pro-inflammatory mediators including NO and PGE2, which was associated with decreased inducible NO synthase and cyclooxygenase-2 expression. ALA also inhibited the LPS-induced expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, reducing their extracellular secretion. Additionally, ALA abolished ROS generation, improved the mitochondrial mass, and enhanced the expression of heme oxygenase-1 (HO-1) and the activation of nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) in LPS-stimulated RAW 264.7 macrophages. However, zinc protoporphyrin, a specific inhibitor of HO-1, reversed the ALA-mediated inhibition of pro-inflammatory cytokines production and activation of mitochondrial function in LPS-treated RAW 264.7 macrophages. Furthermore, ALA significantly abolished the expression of LPS-induced pro-inflammatory mediators and cytokines, and showed strong protective effects against NO and ROS production in zebrafish larvae. In conclusion, our findings suggest that ALA exerts LPS-induced anti-inflammatory and antioxidant effects by upregulating the Nrf2/HO-1 signaling pathway, and that ALA can be a potential functional agent to prevent inflammatory and oxidative damage.