• The Journal of Korean Medicine
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• v.26 no.4
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• pp.152-161
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• 2005

The excessive release of proinflammatory products by activated microglia causes neurotoxicity, and this has been implicated in the pathogenesis of neurodegenerative diseases. Harpagophytum procumbens (Pedaliaceae) has been widely used for the treatment of pain and arthritis in the clinical field. In this study, we investigated the effect of Harpagophytum procumbens against lipopolysaccharide-induced inflammation. From the present results, the aqueous extract of Harpagophytum procumbens was shown to suppress prostaglandin-E2 synthesis and nitric oxide production by inhibiting the lipopolysaccharide-stimulated enhancement of cyclooxygenase-2 and inducible nitric oxide synthase expressions in mouse BV2 microglial cells. These results suggest that Harpagophytum procumbens may offer a valuable means of therapy for the treatment of brain inflammatory diseases by attenuating lipopolysaccharide-induced prostaglandin-E2 synthesis and nitric oxide production.

• Journal of Microbiology and Biotechnology
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• v.11 no.3
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• pp.355-361
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• 2001

A Chromate tolerant strain of Pseudomonas aeruginosa isolated from the effluent of a tannery showed significant enzymatic activity of chromate reduction. Cells grown in chromate-supplemented medium reduced 8 $\mu\textrm{g}$ chromate/mg protein/h in the presence of NADH/NADPH. The chromate reducing activity was inducible as cells pregrown in chromate showed higher chromate reduction. In contrast, the periplasmic fraction of cells gown in chromate reduce $75\%$ chromate in 4 h and the spheroplast fraction failed to do so, indicating that chromate reductase may be located in the periplasm. The presence of a 30 kDa protein in the periplasmic extracts of cells grown in the presence of chromate, but its absence of the protein in cells grown without chromate, points out a possible role of this protein in chromate reduction.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.2
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• pp.111-120
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• 2013

Prolyl 4 hydroxylases (P4H) are iron- and 2-oxoglutamate-dependent dioxygenase enzymes and hypoxia-inducible transcription factor (HIF)-P4Hs play a critical role in the regulating oxygen homeostasis in the local tissues as well in the systemic circulation. Over a period of time, a number of prolyl hydroxylase inhibitors and activators have been developed. By employing the pharmacological tools and transgenic knock out animals, the critical role of these enzymes has been established in the pathophysiology of number of diseases including myocardial infarction, congestive heart failure, stroke, neurodegeneration, inflammatory disease, respiratory diseases, retinopathy and others. The present review discusses the different aspects of these enzymes including their pathophysiological role in disease development.

• Biotechnology and Bioprocess Engineering:BBE
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• v.5 no.4
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• pp.247-252
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• 2000

The strength and regulatory characteristics of the heat-inducible HSA1, HSA2 and TPS1 promoters were compared with those of the well-established, carbon source-regulated FMD promoter in a Hansenula polymorpha-based host system in vivo. In addition, the Saccharomyces cerevisiae-derived ADH1 promoter was analysed. While ADH1 promoter showed to be of poor activity in the foreign host, the strength of the heat shock TPS1 promoter was found to exceed that of the FMD promoter, which at present is considered to be the strongest promoter for driving heterologous gene expression in H. polymorpha.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.5
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• pp.283-287
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• 2003

While nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) is beneficial for host survival, it is also detrimental to the host. Thus, regulation of iNOS gene expression may be an effective therapeutic strategy for the prevention of unwanted reactions at various pathologic conditions. During the screening process for the possible iNOS regulators, we observed that esculetin is a potent inhibitor of cytokine-induced iNOS expression. The treatment of 3T3-L1 adipocytes with the tumor necrosis factor-${\alpha}$ (TNF) induced iNOS expression, leading to enhanced NO production. TNF-induced NO production was inhibited by esculetin in a dose-dependent manner. Esculetin inhibited the TNF-induced NO production at the transcriptional level through suppression of iNOS mRNA and subsequent iNOS protein expression. These results suggest esculetin, a component of natural products, as a naturally occurring, nontoxic means to attenuate iNOS expression and NO-mediated cytotoxicity.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.6
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• pp.479-485
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• 2001

The existence of opioid receptors in mammalian cerebellum except human, has not been clearly understood. In the present study, we found that NPY was inducible by morphine in the mouse cerebellar granular and Purkinje cell layers. We performed in situ RT-PCR and immunohistochemistry to characterize the NPY expression. The increase of NPY gene expression by morphine (30 mg/kg, i.p.) was inhibited by pretreatment with not only naloxone (100 mg/kg, i.p.) but also a noncompetitive NMDA antagonist, MK-801 (0.3 mg/kg, i.p.). The competitive NMDA antagonist, AP-5 (0.9 mg/kg, i.p.) slightly attenuated the increased NPY expression by morphine. Also, the finding similar to morphine was shown by NMDA (70 mg/kg, i.p.) treatment. Our results indicate that NPY was inducible by morphine and this might reflect activation of NMDA receptors in granule cells that relay mossy fiber inputs to Purkinje cells via parallel fibers.

• Journal of Applied Biological Chemistry
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• v.43 no.1
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• pp.12-17
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• 2000

To understand the signal transduction pathway that leads to the activation of the wound-inducible proteinase inhibitor II (pin2) promoter. $F_2$ progenies of wound (-) mutant crossed with wild-type Arabidopsis plants were biochemically and genetically characterized. Wound (-) mutant was derived from transgenic Arabidopsis plants containing bacterial cytosine deaminase gene under the control of pin2 promoter. The cytosine deaminase assays indicated that wound (-) mutant is a dominant inhibitor of wound-inducibility as only 3 of the $20F_2$ progenies showed cytosine deaminase (CDase) activity, To construct a structural map of the wound (-) mutant chromosomal regions, cleaved, amplified polymorphic sequences (CAPS) markers that cover all Chromosomes were used. Chromosomal regions covered by three different CAPS markers could be candidates for further fine mapping of the location of the wound (-) mutation. g4026, RGA1 and ASA1 located at 84.9 on recombinant inbred (RI) map of chromosome I, at 1.75 on RI map of chromosome II, and 18.35 on RI map of chromosome V, respectively.

• Journal of Microbiology
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• v.41 no.3
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• pp.175-182
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• 2003

Production of ribosomally synthesized antimicrobial peptides usually referred to as bacteriocins is an inducible trait in several gram positive bacteria, particularly in those belonging to the group of lactic acid bacteria. In many of these organisms, production of bacteriocins is inducible and induction requires secretion and extracellular accumulation of peptides that act as chemical messengers and trigger bacteriocin production. These inducer peptides are often referred to as autoinducers and are believed to permit a quorum sensing-based regulation of bacteriocin production. Notably, the peptides acting as autoinducers are dedicated peptides with or without antimicrobial activity or the bacteriocins themselves. The autoinducer-dependent induction of bacteriocin production requires histidine protein kinases and response regulator proteins of two-component signal transduction systems. The current working model for the regulation of class II bacteriocin production in lactic acid bacteria and the most relevant direct and indirect pieces of evidence supporting the model are discussed in this minireview.

• Toxicological Research
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• v.3 no.2
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• pp.121-128
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• 1987

Protective effect of scoparone against the acetaminophen inducible hepatic toxicity in mice was investigated. Scoparone (5mg/kg) was administered intraperitoneally to mice daily for 5 days. Scoparone pretreatment before the administration of acetaminophen has blocked subsequent increases in liver to body weight ratio. When biological changes were measured, scoparone protects against acetaminophen inducible hepatotoxicity in mice as evidenced by the decreased formation of lipid peroxide, lowered serum transaminase activity and the decreased level of serum acetaminophen. In conjuction with the results of Huh (Arch. Pharm. Res. 10, 165(1987)), these results suggest that the most likely mechanism for the observed protective effects of scoparone against the acetaminophen-induced hepatotoxicity is the induction of hepatic microsomal UDP-glucuronyltransferase activity.

• Korean Journal of Veterinary Research
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• v.53 no.4
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• pp.225-230
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• 2013

To better understand the role of macrophages in early stages of experimental autoimmune myocarditis (EAM), we compared the expression of inducible nitric oxide synthase (iNOS) and arginase-1, markers for classically activated M1 and alternatively activated M2 macrophages, respectively, in the hearts of EAM-affected and control rats. Immunohistochemical evidence revealed that both iNOS-positive and arginase 1-positive macrophages were found in EAM lesions, while some cells were co-localized with both markers. This finding suggests that the increased level of arginase-1, which is partly from M2 macrophages, contributes to the modulation of EAM, possibly through the reduction of nitric oxide in the lesion.