• Archives of Pharmacal Research
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• v.19 no.2
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• pp.160-162
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• 1996

The structural analysis of tolfenamic acid, 2-[(3-chloro-2-methylphenyl)-amino]benzoic acid, was performed by single crystal X-ray diffraction technique. The compound was recrystallized from a mixture of ether and toluene in triclinic, space group $P2_1/c, \;with\; \partial=3.914(1), \; b=22.\; 020(2), \; c=14.271(1)\;{\AA}, \beta.=94.68(1)^{\circ}, $ and Z=4. The calculated density is $1.418 g/cm^3$. The structure was solved by the direct method and refined by full matrix least-squares procedure to the final R value of 0.039 for 1773 independent reflections. In the molecule, carboxyl group at the anthranilic acid is coplanar to the phenyl ring. The dihedral angle between the two aromatic rings of the molecule is $44.2^{\circ}$ The molecules are dirnerized through the intermolecular hydrogen bonds at the carboxyl group in the crystal.

• Biomolecules & Therapeutics
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• v.23 no.1
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• pp.39-44
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• 2015

Tolfenamic acid (TA) is a traditional non-steroid anti-inflammatory drug (NSAID) and has been broadly used for the treatment of migraines. Nuclear factor kappa B (NF-${\kappa}B$) is a sequence-specific transcription factor and plays a key role in the development and progression of inflammation and cancer. We performed the current study to investigate the underlying mechanisms by which TA suppresses inflammation focusing on NF-${\kappa}B$ pathway in TNF-${\alpha}$ stimulated human normal and cancer cell lines and lipopolysaccharide (LPS)-stimulated mouse macrophages. Different types of human cells (HCT116, HT-29 and HEK293) and mouse macrophages (RAW264.7) were pre-treated with different concentrations of TA and then exposed to inflammatory stimuli such as TNF-${\alpha}$ and LPS. Transcriptional activity of NF-${\kappa}B$, $l{\kappa}B-{\alpha}$-degradation, p65 translocation and mitogen-activated protein kinase (MAPK) activations were measured using luciferase assay and Western blots. Pre-treatment of TA repressed TNF-${\alpha}$- or LPS-stimulated NF-${\kappa}B$ transactivation in a dose-dependent manner. TA treatment reduced degradation of $l{\kappa}B-{\alpha}$ and subsequent translocation of p65 into nucleus. TA significantly down-regulated the phosphorylation of c-Jun N-terminal kinase (JNK). However, TA had no effect on NF-${\kappa}B$ signaling and JNK phosphorylation in HT-29 human colorectal cancer cells. TA possesses anti-inflammatory activities through suppression of JNK/NF-${\kappa}B$ pathway in different types of cells.

• Korean Journal of Veterinary Service
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• v.34 no.3
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• pp.285-289
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• 2011

This study was conducted to determine the content of non-steroidal anti-inflammatory drugs (NSAIDs) in meats available on the Korean markets. The analysis was carried out using following conditions; C18 column ($100{\times}2.1$ mm, 1.7 ${\mu}m$), mobile phase composed of DW (containing 0.1% formic acid): acetonitrile (containing 0.1% formic acid), binary pump at a flow rate of 0.3 ml/min and 5 ${\mu}l$ of injection volume, MS/MS detector with ESI positive mode. The calibration range of five NSAIDs showed linearity ($r^2{\geq}0.99$) at concentration range of 3.125~200 ${\mu}g$/kg. The recoveries in fortified muscle more than 78.7~100.3%. The detection limits for meloxicam, ketoprofen, flunixin, carprofen and tolfenamic acid were 3.5, 1.6, 1.7, 9.8 and 4.8 ${\mu}g$/kg, respectively. We also monitored NSAIDs residue in cattle muscle 51 samples. The test results, NSAIDs were all not founded.

• Journal of Life Science
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• v.32 no.1
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• pp.23-28
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• 2022

CopA3 (LLCIALRKK), an antimicrobial peptide isolated from the Korean dung beetle, has been shown to suppress apoptosis in various cell types. CopA3 inhibits not only bacterial toxin-induced colonocyte apoptosis but also 6-hydroxy dopamine-induced neural cell apoptosis. Our recent study revealed that CopA3 directly binds to caspases (key regulators of apoptosis) and inhibits the proteolytic cleavage required for their activation. But molecular mechanisms underlying CopA3-mediated inhibition of apoptosis in multiple cell types remain unknown. Here we assessed possible effects of CopA3 on expression of survivin, which is known to inhibit apoptosis. In HT29 human colonocytes, CopA3 exposure markedly upregulated survivin expression in a concentration- and time-dependent manner. RT-PCR revealed that CopA3-mediated upregulation of survivin was attributable to increased gene transcription, and further showed that CopA3 also increased expression of Sp1, one of many transcription factors known to be involved in transcription of the survivin gene. Notably, blocking Sp1 by treatment with the Sp1 inhibitor, tolfenamic acid, significantly reduced CopA3-mediated upregulation of survivin. These results collectively suggest that CopA3 induces Sp1 expression, which in turn is involved in upregulation of survivin in human colonocytes. These novel findings establish another pathway for explaining the anti-apoptotic effects of CopA3 against various cellular apoptosis systems.

• Animal Bioscience
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• v.36 no.8
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• pp.1293-1303
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• 2023

Objective: Inflammation and pain management in postpartum hyperprolific sows is currently an important animal welfare issue in the swine industry. The present study investigates effects of ketoprofen treatment on the incidence of post-parturient disorders, feed intake, colostrum yield, piglet colostrum intake, colostrum immunoglobulin G (IgG) and piglet mortality rate during the first 3 days of postnatal life. Methods: In total, 61 Danish Landrace×Yorkshire crossbred sows and their offspring (n = 833) were included in the experiment. The sows were randomly distributed into two groups: i) control (n = 31), sows were treated with tolfenamic acid 2 mg per kg for 2 days postpartum; ii) ketoprofen (n = 30), sows were treated with ketoprofen 3 mg per kg for 2 days postpartum. The farrowing process of the sows was monitored for 24 h daily, and data associated with farrowing were collected. Piglet colostrum intake, sow colostrum yield and colostrum IgG were determined. Results: During the first 3 days postpartum, the incidence of sows that had fever did not differ between control and ketoprofen groups (51.6% and 56.7%, respectively, p = 0.692). Piglet colostrum intake did not differ between control and ketoprofen groups (p = 0.736). However, the proportions of piglets that had inadequate colostrum intake were 71.3%, 22.6%, and 5.4% in those with birth weights of <1.0 kg, 1.0 to 1.29 kg, and ≥1.30 kg, respectively (p<0.001). The piglet mortality rate did not differ between control and ketoprofen groups (p = 0.808). Conclusion: Administration of ketoprofen in postpartum sows for 2 days can control the evidence of post-parturient disorders in sows as effectively as the use of tolfenamic acid. No deleterious effect of ketoprofen was detected on sow colostrum yield, piglet colostrum intake and piglet mortality. Therefore, ketoprofen can be recommended as an alternative anti-inflammatory drug used in postpartum sows.