• Title/Summary/Keyword: Anti-inflammatory inhibitors

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Comparison of safety and analgesic efficacy of diclofenac sodium with etodolac after surgical extraction of third molars: a randomized, double-blind, double-dummy, parallel-group study

  • Vaghela, Jitendra H.;Shah, Jigna H.;Patel, Jaladhi H.;Purohit, Bhargav M.
    • Journal of Dental Anesthesia and Pain Medicine
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    • v.20 no.1
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    • pp.19-27
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    • 2020
  • Background: Surgical extraction of third molars is associated with postoperative pain and swelling at the extraction site. Pain is commonly managed using non-steroidal anti-inflammatory drugs (NSAIDs). Postoperative pain is usually moderate to severe in the first 12 h postoperatively and lasts for 3-5 days. However, with NSAIDs, these symptoms usually subside within 24 h. Diclofenac sodium and etodolac are NSAIDs, more selectively cyclooxygenase-2 inhibitors, with good analgesic efficacies. Methods: We compared the safety and analgesic efficacy of diclofenac sodium with etodolac peroral after surgical extraction of third molars in a double-blind, double-dummy, parallel-group study. The subjective pain improvement and pain relief after 2, 6, 24, 48, and 72 h using the visual analogue scale were measured as the study outcome. Results: Etodolac was equivalent to diclofenac sodium in pain alleviation at all postoperative time periods. No significant differences were found between diclofenac sodium and etodolac groups (P > 0.05). Both study medications were well tolerated and safe with mild adverse effects in only a few participants. Conclusion: Diclofenac sodium and etodolac are comparable in terms of analgesic efficacy and safety after surgical removal of third molars.

Pinosylvin exacerbates LPS-induced apoptosis via ALOX 15 upregulation in leukocytes

  • Kwon, Ohseong;Seo, Youngsik;Park, Heonyong
    • BMB Reports
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    • v.51 no.6
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    • pp.302-307
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    • 2018
  • Pinosylvin is known to have anti-inflammatory activity in endothelial cells. In this study, we found that pinosylvin had a pro-apoptotic activity in lipopolysaccharide (LPS)-preconditioned leukocytes. This finding suggests that pinosylvin has an effect on the resolution of inflammation. To understand the detailed mechanism, we examined if pinosylvin enhances cyclooxygenase (COX) or lipoxygenase (LOX) activity in THP-1 and U937 cells. LOX activity was found to be markedly increased by pinosylvin, whereas COX activity was not altered. Furthermore, we found that pinosylvin enhanced both levels of ALOX 15 mRNA and protein, implying that LOX activity, elevated by pinosylvin, is attributed to upregulation of ALOX 15 expression. From this cell signaling study, pinosylvin appeared to promote phosphorylations of ERK and JNK. ERK or JNK inhibitors were found to attenuate ALOX 15 expression and LPS-induced apoptosis promoted by pinosylvin. In conclusion, pinosylvin enhances the apoptosis of LPS-preconditioned leukocytes by up-regulating ALOX 15 expression through ERK and JNK. These findings suggest that pinosylvin may induce the resolution of inflammation.

Suppressive effects of pinosylvin on prostaglandin E$_2$and nitric oxide production in lipopolysaccharide-stimulated RAW 264.7 cells

  • Park, Eun-Jung;Min, Hye-Young;Kim, Moon-Sun;Pyee, Jae-Ho;Ahn, Yong-Hyun;Lee, Sang-Kook
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2003.11a
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    • pp.102-102
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    • 2003
  • The inhibitors of prostaglandin biosynthesis and nitric oxide production by corresponding inducible isozyme have been considered as potential anti-inflammatory and cancer chemopreventive agents. In our continuous search for cancer chemopreventive agents from natural products, we have evaluated the inhibitory potential of PGE$_2$and NO production in lipopolysaccharide (LPS)-induced mouse macrophage RAW264.7 cells. As a result, pinosylvin (3,5-dihydroxy-trans-stilbene), a stilbenoid, mainly found from the heartwood and leaves of the Pinus sylvestris, showed potential inhibitory activity of LPS-induced PGE$_2$and NO production in a dose-dependent manner. Pinosylvin also suppressed the LPS-induced iNOS protein expression. Further study revealed that pinosylvin exhibited antioxidant activity by the DPPH free radical scavenging potential and inhibitory effect of xanthine oxidase activity. In addition, pinosylvin inhibited COX -2 overexpressed human colon cancer cell (HT-29) growth in a time- and dose-dependent manner. These findings suggest that pinosylvin might be a promising candidate for developing cancer chemopreventive agent.

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Assay System for N-acylethanolamines Degradation Enzyme, N-acylethanolamine-hydrolyzing Acid Amidase

  • Kim, Dae-Woong;Kim, Gun-Joong;Kim, Hae-Jo;Ghil, Sung-Ho
    • Biomedical Science Letters
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    • v.18 no.4
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    • pp.438-444
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    • 2012
  • N-acylethanolamines (NAEs) including endocannabinoids, anadamide, are long chain fatty acid ethanolamines and express ubiquitously in animal and plant tissues. NAEs have several pharmacological effects including anti-inflammatory, analgesic and anorexic effects. The levels of NAEs in tissues are strictly regulated by synthesizing and hydrolyzing enzymes because NAEs are not stored in the cell but rather made on demand. NAEs are hydrolyzed to free fatty acids and ethanolamines by fatty acid amide hydrolase and N-acylethanolamine-hydrolyzing acid amidase (NAAA). Here, we suggest the fluorescence-based assay system for NAAA. We developed N-(4-methy-2-oxo-2H-chromen-7-yl)palmitamide (PAAC) as a fluorogenic substrate for NAAA and we also generated NAAA stably expressing COSM6 cell line. When extracts of cells expressing NAAA were incubated with PAAC, NAAA specifically hydrolyzed PAAC to palmitic acids and fluorogenic dye, coumarin. Release of coumarin was monitored by using fluorometer. NAAA hydrolyzed PAAC with an apparent Km of $20.05{\mu}M$ and Vmax of 32.18 pmol/mg protein/min. This assay system can be used to develop inhibitors or activators of NAAA.

Inhibitors of Nitric Oxide Syntheasis from Phellinus pini in Murine Macrophages (낙엽송층버섯의 Nitric Oxide 생성저해 물질)

  • Jang, Hyun-Jin;Kim, Ahn-Keun;Pyo, Myoung-Yun;Yang, Ki-Sook
    • YAKHAK HOEJI
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    • v.51 no.6
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    • pp.430-434
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    • 2007
  • The anti-inflammatory activity of fruit body of Phellinus pini was investigated by activity-guided fractionation. From the screening of each fraction for the inhibitory activity of NO production in lipopolysaccaride (LPS) activated RAW 264.7 cells, methanol extract and its hexane soluble fraction of Phellinus pini exhibited inhibition of NO production compared with LPS control without toxicity. The hexane soluble fraction showed dose-dependent inhibition of NO production. The active hexane fraction was repeatedly chromatographed over silica gel, ergosta-7,24(28)-dien-3-ol(1) and ergosterol peroxide (2) were isolated and identified. Ergosterol derivatives were inhibited NOS activation, $IC_{50}$ of them were $18.9{\pm}3.9{\mu}M$ (1) and $20.4{\pm}4.5{\mu}M$ (2).

Lipoxygenase Inhibitors from Paeonia lactiflora Seeds

  • Kim, Hyo-Jin;Chung, Shin-Kyo;Park, Sang-Won
    • Preventive Nutrition and Food Science
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    • v.4 no.3
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    • pp.163-166
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    • 1999
  • Previously, the methanolic extract of Paeonia lactiflora seeds was shown to have strong ingibitory activity against soybean liposygenase (SLO). Four phenolic compounds were isolated from the seeds by solvent fractionation Sephadex LJ-20 column chromatography and preparative HPLC, and three of them showed strong SLO inhibitio and were characterized as trans-resveratrol, $\varepsilon$-viniferin and luteolin by UV, IR, 1H-NMR, 13C-NMR and MS spectrometry. trans-Resveratrol (IC50=1.02$\mu$M), $\varepsilon$-viniferin (IC50=0.81$\mu$M) and luteolin (IC50=10.01$\mu$M), first found in the above seeds, exhibited a potent SLO inhibitory activity although their activity was lower than that of a well-known lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA) (IC50=0.57$\mu$M). These results suggest that Paenia lactiflora seeds, now an unused plant seed, may be developed into useful sources of anti-inflammatory drugs.

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A Novel Homozygous CLCNKB Mutation of Classic Bartter Syndrome Presenting with Renal Cysts in 6-year-Old Identical Twin Boys : A Case Report

  • Son, Min Hwa;Yim, Hyung Eun;Yoo, Kee Hwan
    • Childhood Kidney Diseases
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    • v.25 no.1
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    • pp.35-39
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    • 2021
  • Bartter syndrome is an autosomal recessive hypokalemic salt-losing tubulopathy, and classic Bartter syndrome is associated with mutations in the CLCNKB gene. While chronic hypokalemia is known to induce renal cyst formation in different renal diseases, renal cyst formation in Bartter syndrome is rarely reported. Russian six-year-old identical male twins were referred to our hospital for the evaluation of renal cysts, which were incidentally detected on abdominal sonography due to diarrhea. Both twins had shown symptoms of polydipsia, polyuria, and nocturia since they were one year olds. Vital signs including blood pressure were normal in both twins. Renal sonography revealed nephromegaly, increased echogenicity of renal cortex, and various sized multiple cysts in both kidneys for both twins. Laboratory findings included hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. Bartter syndrome with renal cysts were suspected. Genetic analysis for both twins confirmed a homozygous c.1614delC deletion on exon 15 of the CLCNKB gene, which was confirmed as a previously unreported variant to the best of our knowledge. They were managed with potassium chloride, nonsteroidal anti-inflammatory drugs, and angiotensin-converting-enzyme inhibitors. Metabolic alkalosis, hypokalemia, hypochloremia, and polyuria partially improved during the short course of treatment. This is the first report of a homozygous mutation in the CLCNKB gene in an identical twin, presenting with renal cysts.

The Cholesterol-Binding Antibiotic Nystatin Induces Expression of Macrophage Inflammatory Protein-1 in Macrophages

  • Baek, Seungil;Kim, Sun-Mi;Lee, Sae-A;Rhim, Byung-Yong;Eo, Seong-Kug;Kim, Koanhoi
    • Biomolecules & Therapeutics
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    • v.21 no.1
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    • pp.42-48
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    • 2013
  • Nystatin, a polyene antifungal antibiotic, is a cholesterol sequestering agent. The antifungal agent alters composition of the plasma membrane of eukaryotic cells, whereas its effects on cells are poorly investigated. In the current study, we investigated the question of whether nystatin was able to induce expression of macrophage inflammatory protein-1 (MIP-1). THP-1 cells rarely express MIP-$1{\alpha}$ and MIP-$1{\beta}$, however, upon exposure to nystatin, significantly elevated expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed in a dose-dependent fashion at the messenger and protein levels. Cellular factors activated by nystatin as well as involved in nystatin-induced expression of MIP-1 proteins were identified in order to understand the molecular mechanisms of action of the anti-fungal agent. Treatment with nystatin resulted in enhanced phosphorylation of Akt, ERK, p38 MAPK, and JNK. Abrogation or significant attenuation of nystatin-induced expression of MIP-$1{\alpha}$ and MIP-$1{\beta}$ was observed by treatment with Akt inhibitor IV, LY294002, and SP6001250. Inhibition of ERK or p38MAPK using U0126 and SB202190 did not lead to attenuation of MIP-1 expression. In addition, inhibitors of protein kinase C, such as GF109203X and Ro-318220, also attenuated expression of MIP-1. These results indicate that nystatin is able to activate multiple cellular kinases and, among them, Akt and JNK play primary roles in nystatin-induced expression of MIP-1 proteins.

Atopic Dermatitis-Related Inflammation in Macrophages and Keratinocytes: The Inhibitory Effects of Bee Venom

  • Kim, Deok-Hyun;Song, Ho-Sueb
    • Journal of Acupuncture Research
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    • v.36 no.2
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    • pp.80-87
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    • 2019
  • Background: This study investigated the anti-inflammatory effects of bee venom (BV) through the inhibition of nuclear factor kappa beta ($NF-{\kappa}B$) expression in macrophages and keratinocytes. Methods: Cell viability assays were performed to investigate the cytotoxicity of BV in activated macrophages [lipopolysaccharide (LPS)] and keratinocytes [interferon-gamma/tumor necrosis factor-alpha ($IFN-{\gamma}/TNF-{\alpha}$)]. A luciferase assay was performed to investigate the cellular expression of $NF-{\kappa}B$ in relation to BV dose. The expression of $NF-{\kappa}B$ inhibitors ($p-I{\kappa}B{\alpha}$, $I{\kappa}B{\alpha}$, and p50 and p65) were determined by Western Blot analysis, and the electromobility shift assay. A nitrite quantification assay was performed to investigate the effect of BV, and $NF-{\kappa}B$ inhibitor on nitric oxide (NO) production in macrophages. In addition, Western Blot analysis was performed to investigate the effect of BV on the expression of mitogen-activated protein kinases (MAPK) in activated macrophages and keratinocytes. Results: BV was not cytotoxic to activated macrophages and keratinocytes. Transcriptional activity of $NF-{\kappa}B$, and p50, p65, and $p-I{\kappa}B{\alpha}$ expression was reduced by treatment with BV in activated macrophages and keratinocytes. Treatment with BV and an $NF-{\kappa}B$ inhibitor, reduced the production of NO by activated macrophages, and also reduced $NF-{\kappa}B$ transcriptional activity in activated keratinocytes (compared with either BV, or $NF-{\kappa}B$ inhibitor treatment). Furthermore, BV decreased p38, p-p38, JNK, and p-JNK expression in LPS-activated macrophages and $IFN-{\gamma}/TNF-{\alpha}$-activated keratinocytes. Conclusion: BV blocked the signaling pathway of $NF-{\kappa}B$, which plays an important role in the inflammatory response in macrophages and keratinocytes. These findings provided the possibility of BV in the treatment of atopic dermatitis.

Atorvastatin and Fluvastatin Can Reduce IL-1β-induced Inflammatory Responses in Human Keratinocytes (Atorvastatin 그리고 fluvastatin 약물의 IL-1β-유도 염증반응 억제 효과)

  • Choe, Yeong-In;Moon, Kyoung Mi;Yoo, Jae Cheal;Byun, June-Ho;Hwang, Sun-Chul;Moon, Dong Kyu;Woo, Dong Kyun
    • Journal of Life Science
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    • v.31 no.4
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    • pp.418-424
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    • 2021
  • Skin inflammation (dermatitis) is caused by varying skin damage due to ultraviolet radiation and microbial infection. Currently prescribed drugs for dermatitis include anti-histamine and steroid drug classes that soothe inflammation. However, incorrect or prolonged use of steroids can cause weakening of skin barriers as well as osteoporosis. Therefore, treating dermatitis with a drug that has minimal side effects is important. Statins, also known as 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, are cholesterol-lowering drugs that have been widely treated for hyperlipidemia and cardiovascular diseases. Interestingly, recent studies have shown the anti-inflammatory effects of statins in both experimental and clinical models for of osteoarthritis. This study investigated the possible anti-inflammatory effects of atorvastatin and fluvastatin in human keratinocytes (HaCaT cells), which are crucial components of skin barriers. Stimulation of HaCaT cells with IL-1β increased the expression of the COX2 protein, a major player of inflammatory responses. However, this induction of the COX2 protein was downregulated by pretreatments with atorvastatin and fluvastatin. Treatment with IL-1ß-induced the upregulation of other inflammatory genes (such as iNOS and MMP-1) and these expressions were similarly lowered by these two statin drug treatments. Taken together, these results indicated that atorvastatin and fluvastatin can reduce IL-1β-induced inflammatory responses in HaCaT cells. In conclusion, the findings suggest that atorvastatin and fluvastatin can be potential modulators for ameliorating skin inflammation.