• Korean Journal of Pharmacognosy
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• v.48 no.1
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• pp.31-37
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• 2017

Glutamate-induced oxidative stress results in neuro-degenerative disorders in many central nervous system (CNS) such as Alzheimer's disease, ischemia, Huntington's disease, and Parkinson's disease. Our study was performed to investigate neuroprotective effects of Allium hookeri extracts (leaf, root, and whole) on glutamate-induced HT22 cells. In this study, ethanol extract of A. hookeri showed the outstanding neuroprotective effect in HT22 cells. In addition, we found that ethanol extract of A. hookeri root increased heme oxygenase (HO)-1 in HT22 cells. Moreover, ethanol extract of A. hookeri root also upregulated nuclear accumulation of nuclear factor E2-related factor 2 (Nrf2) in HT22 cells. These results demonstrate that ethanol extract of A. hookeri root contributes neuroprotective effects against glutamate-induced oxidative stress in HT22 cells, via Nrf2-mediated HO-1 expression. Our study suggests that ethanol extract of A. hookeri root could be the potential agent for the treatment of many neuro-degenerative diseases.

• Journal of Life Science
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• v.12 no.5
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• pp.561-565
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• 2002

Pseudomonas sp. EL-041 was previously isolated from phenol-acclimated activated sludge. This bacterium was capable of degrading phenol and cometabolizing trichloroethylene (TCE). In this study, we report the identification of trichloroethylene- degrading enzyme in Pseudomonas sp. EL-041 by the investigation of enzyme activity and DNA sequencing of specific phenol oxygenase gene. As the results of experiment, trichloroethylene-degrading enzyme in Pseudomonas sp. EL-041 was monooxygenase and suspected to phenol hydroxylase.

• Archives of Pharmacal Research
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• v.25 no.3
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• pp.343-348
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• 2002

Carbon monoxide (CO) are produced by heme oxygenase (HO), and HO was detected in hypothalamus. However, the roles of CO produced in hypothalamus was not fully elucidated. So, we tested the effects of CO on body temperature because preoptic-anterior hypothalamus was known as the presumptive primary fever-producing site. CO-saturated aCSF ($4{\;}{\mu}l$, i.c.v.) and hemin ($10{\;}{\mu}g$, i.c.v.) elicited marked febrile response. Pretreatment with indomethacin completely inhibited CO- and hemin-induced fever. Zinc protoporphyrin-IX ($10{\;}{\mu}g$, i.c.v.) or ODQ ($50{\;}{\mu}g$, i.c.v.) partially reduced hemin-induced febrile response. Dibutyryl-cGMP ($100{\;}{\mu}g$, i.c.v.) produced profound febrile response and this febrile response was attenuated by indomethacin. These results indicate that endogenous CO may have a role as a pyrogenic mediator in CNS and CO-mediated pyresis is dependent on prostaglandin production and partially on activation of soluble guanylate cyclase.

• Korean Journal of Pharmacognosy
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• v.45 no.2
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• pp.161-167
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• 2014

Ganoderma lucidum L. (GL) is a traditional oriental medicine that has been widely used as anti-inflammatory, antitumor and anti-oxidant in Korea and other Asian countries. In this study, we investigated the ethanol extract of GL has neuroprotective effects in murine hippocampal HT22 cells. GL ethanol extract has the potent neuroprotective effects on glutamate-intoxicated cells by inducing the expression of heme oxygenase (HO)-1 in HT22 cells. GL ethanol extract increased JNK phosphorylation. Obviously, When we treated the GL extract with c-Jun N-terminal kinase (JNK) inhibitor (SP600125), HO-1 expression was reduced. Moreover, we found that GL treatment caused the nuclear accumulation of Nrf2. In conclusion, the ethanol extract of GL significantly protects glutamate-induced oxidative damage by induction of HO-1 via Nrf2, JNK pathway in mouse hippocampal HT22. These results suggest that GL ethanol extract would be a good source for taking active compounds and may be a potential pharmaceutical products for brain disorder induced by neuronal damage and oxidative stress.

• BMB Reports
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• v.50 no.4
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• pp.220-225
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• 2017

Antisense transcripts were initially identified as transcriptional noise, but have since been reported to play an important role in the quality control of miRNA functions. In this report, we tested the hypothesis that heterogeneous nuclear ribonucleoprotein K (hnRNPK) regulates miRNA function via competitive endogenous RNAs, such as pseudogenes, long non-coding RNAs, and antisense transcripts. Based on analyses of RNA sequencing data, the knockdown of hnRNPK decreased the antisense PTOV1-AS1 transcript which harbors five binding sites for miR-1207-5p. We identified heme oxygenase-1 (HO-1) mRNA as a novel target of miR-1207-5p by western blotting and Ago2 immunoprecipitation. The knockdown of hnRNPK or PTOV1-AS1 suppressed HO-1 expression by increasing the enrichment of HO-1 mRNA in miR-1207-5p-mediated miRISC. Downregulation of HO-1 by a miR-1207-5p mimic or knockdown of hnRNPK and PTOV1-AS1 inhibited the proliferation and clonogenic ability of HeLa cells. Taken together, our results demonstrate that hnRNPK-regulated PTOV1-AS1 modulates HO-1 expression via miR-1207-5p.

• Herbal Formula Science
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• v.16 no.2
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• pp.193-204
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• 2008

Dehydrocostus lactone (DHL) and Mokko lactone (ML) were isolated from Saussureae Radix, and their effects on heme oxygenase-1 (HO-1) expression and hepatoprotection in the liver cell line HepG2 were investigated. DHL induced HO-1 expression and HO activity in a dose-dependent manner, whereas ML lacking one double bond property at 11 and 13 carbons on its own chemical structure had no apparent effects. DHL also induced Nrf2 nuclear translocation and enhanced antioxidant response element (ARE) activation which mediated HO-1 gene transcription. Pretreatment with DHL protected HepG2 cells against oxidative damages caused by H2O2. Interestingly, the hepatoprotective effects of DHL appeared to be associated with HO enzymatic activation, HO-1 expression and Nrf2 activation, because blockage of HO activity by a HO inhibitor and inhibition of HO-1 and Nrf2 cellular synthesis by small interfering RNA abolished heptoprotection afforded by DHL. Taken together, this investigation provides evidence supporting that Saussureae Radix is hepatoprotective against oxidative stress that causes abnormal liver damages.

• Toxicological Research
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• v.20 no.4
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• pp.293-298
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• 2004

Background: Crohn's disease is characterized by a chronic relapsing inflammation of the bowel. Gliotoxin has been known to play strong immunosuppressive properties, while mechanisms for its anti-inflammatory actions are not completely understood. Here, we investigated the effects of gliotoxin in trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, an animal model of Crohn's disease. Results: Gliotoxin dramatically improved clinical and histopathological symptoms in accompanied with reduced expression of TNF-$\alpha$, IL-1$\beta$, and ICAM-1 protein levels in TNBS induced colitis. Interestingly Gliotoxin induced Heme oxygenase-1 (HO-1) and the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) completely mimicked the protective effects of gliotoxin in TNBS induced colitis mice. In contrast, the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) could reverse the anti-inflammatory effects of gliotoxin and CoPPIX. Conclusions: Gliotoxin is a potential therapeutic agent targeting for the treatment of Crohn's disease by inducing HO-1.

• Molecules and Cells
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• v.23 no.2
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• pp.198-206
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• 2007

Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, IL-3, IL-6, IL-10, IL-12p40, IL-23], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)] and the activation and expression of CD29 as judged by cell-cell adhesion and surface staining experiments. The inhibition was due to the induction of heme oxygenase (HO)-1 in LPS-activated macrophages, since blocking HO-1 activity with ZnPP, an HO-1 specific inhibitor, abolished hydroquinone's NO inhibitory activity. In addition, hydroquinone and inhibitors (wortmannin and LY294002) of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway had very similar inhibitory effects on LPS-induced and CD29-mediated macrophage responses, including the phoshorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanisms.

• Korean Journal of Microbiology
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• v.29 no.6
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• pp.408-415
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• 1991

TOL plsmid size of Flavobacterium odoratum SUB53 was estimated as 83 Md and the optimum concentration of m-toluate degradation by TOL plasmid was 5 mM. $H_{2}$ production by Rhodopseudomonas sphaeroides KCTC1425 was largely dependent on nitrogenase activity and showed the highest at 30 mM malate with 7 mM glutamate as nitrogen source. Nitrogenase activities were inhibited by 0.3 mM $NH_{4}^{+}$ions, to be appeared the decrease of $H_{2}$ production. Conjugation of TOL plasmids from F. odoratum SUB53 and Pseudomonas putida mt-2 to R. sphaeroides showed the optimum at the exponential stage of recipient cells in presence of helper plasmid pRK2013. According to the investigation of catechol-1,2-oxygenase (C-1, 2-O) and catechol-2,3-oxygenase (C-2,3-O) activities of R. sphaeroides C1 (TOL SUB53) and C2 (TOL mt-2), the gene for C-2,3-O is located on TOL plasmid and gene for C-1, 2-O on the chromosome of R. sphaeroides. m-Toluate was biodegraded by TOL plasmid in R. sphaeroides C1 and C2, presumably to be produced $H_{2}$ gas from the secondary metabolites of m-toluate.e.

• Food Science and Biotechnology
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• v.18 no.5
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• pp.1055-1062
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• 2009

This study was conducted to investigate whether dietary chlorella intake could have an effect on antioxidative capacity in rats oxidatively stressed with cadmium (Cd). Sprague-Dawley rats fed dietary chlorella (0, 5, and 10%) for 4 weeks after induction of oxidative stress by exposing to Cd (200 ppm) for 8 weeks. After the oxidative stress applied, plasma and liver malondialdehyde concentrations and xanthine oxidase activities were decreased in 5% chlorella fed group compared to chlorella free group. Although liver heme oxygenase-1 protein expression was not affected by chlorella, the enzyme activity was improved in 5% chlorella fed group. Erythrocyte superoxide dismutase activity and hepatic metallothionein concentration were increased in 5% chlorella fed group. However, 10% chlorella intake had no effect on the improvement of oxidative stress-related enzymes and proteins. These findings suggest that, after induction of oxidative stress with Cd, 5% chlorella intake might improve antioxidative capacity against oxidative stress.