• Journal of Dental Rehabilitation and Applied Science
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• v.33 no.1
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• pp.7-18
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• 2017

Purpose: Nonsteroidal anti-inflammatory drugs that prohibit biosynthesis of arachidonic acid metabolites have been considered potent host modulation agents. The aim of this review was to determine the effect of nonsteroidal anti-inflammatory drugs adjunctive with nonsurgical periodontal treatment in patients with periodontal disease. Materials and Methods: Three electronic databases were searched to identify relevant studies. The methodological quality and mean differences of the change in clinical attachment level and probing depth were analyzed according to Cochrane review methods. Results: Twelve studies were included in the methodological assessment and nine studies were suitable for inclusion in the meta-analysis. The mean difference in the clinical attachment level gain did not differ significantly between the nonsteroidal anti-inflammatory drugs and control groups at any observation time. The highest mean difference in clinical attachment level gain was 0.30 mm at 4 weeks (95% confidence interval = -0.37 to 0.97). There was a significant mean difference in the probing depth reduction, of 0.34 mm (95% confidence interval = 0.29 to 0.40) at 6 weeks. Conclusion: Therefore, nonsteroidal anti-inflammatory drugs have additional therapeutic effect when administrated with nonsurgical periodontal treatment.

• Korean journal of food and cookery science
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• v.20 no.5
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• pp.505-510
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• 2004

이물질 침입에 대한 인식의 결과 NO, PGE$_2$, TNF-, IL-6와 같은 여러 신호전달물질의 분비가 개시되며 이들을 억제하는 물질을 항염증제라고 볼 수 있다. 본 연구에서는 회향(Foeniculum vulgare Mill.) 열매 추출물이 mouse macrophages RAW264.7 세포에서 lipopolysaccharide(LPS)로 유도한 NO(iNOS 산물), PGE$_2$(COX-2 산물) 및 cytokines (TNF-$\alpha$, IL-6) 생성 억제에 미치는 영향을 살펴보았다. 회향 열매의 methanol 추출물 및 분획물(chloroform, butanol, and aqueous fractions)은 4～100$\mu$g/mL 농도에서 LPS가 활성화된 대식 세포에서 NO 생성을 억제하였으며 독성을 나타내지 않았다. LPS가 유도한 PGE$_2$ 생성은 butanol 분획(100 $\mu$g/mL)에 의해서만 유의적으로 감소하였다(P<0.05). 회향 열매 추출물 및 분획물은 TNF-$\alpha$의 생성을 유의적으로 감소시켰으며 IL-6의 생성은 methanol extract(4～100 $\mu$g/mL), chloroform fraction(4 $\mu$g/mL), butanol fraction(4 and 100$\mu$g/mL) 및 aqueous fraction(4～100 $\mu$g/mL)에 의해 감소되었다(P<0.05). 이는 회향 열매 추출물은 염증 상태에서 유용할 것이며 COX-2와 iNOS를 억제하는 butanol 분획은 새로운 항염증제 개발에 사용될 수 있음을 시사하여 주었다.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.20 no.1
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• pp.25-36
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• 1994

It is weal known that bacterial lipopolysaccharide (LPS) stimulates prostaglandin synthesis in various experimental system via enhancing the expression of cylooxygenase-2 (COX-2). This study was designed to characterize U)5-induced prostaglandin synthesis in mouse peritoneal macrophages LPS-stimulated prostaglandin synthesis in macrophages with short term exposure was not so much prominent, but there was a burst in prostaglandin synthesis 8 hours after the LPS treatment and this u·as accompanied with the increase of cyclooxygenase activity, Dexamethasone markedly inhibited prostaglandin synthesis in this system. Metabolic label ins data supported above observations and thus, it could be concluded that LPS induces the do novo synthesis of COX-2 by which it stimulates the prostaglandin synthesis in mouse peritoneal macrophages, These data suggested that this experimental model system could be used for the screening procedure of COX-2 selective inhibitors. Ketoprofen, a non steroidal anti inflammatory agent, appeared to inhibit COX-1 relatively more selectively than COX-2.

• Applied Chemistry for Engineering
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• v.10 no.1
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• pp.135-137
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• 1999

For the synthesis of new anti-inflammatory agents as indol derivatives, we have synthesized ${\alpha}$-benzoyl-1-ethyl-1,3,4,9-tetrahydro-8-ethyl-9-(N-benzoyl)pyrano[3,4-b]indole-1-acetic acid methyl ester. It was a new method for ${\alpha}$-substituted etodolac carboxylic acid. The synthetic process was composed of four steps, and 7-ethylindole and oxalyl chloride were used as starting materials. The third step, cyclization was carried out by addition of borontrifluoride diethyl etherate in 66% yield. The step of reduction and cyclization were simplified successfully. The final product, ${\alpha}$-benzoyl-1-ethyl-1,3,4,9-tetrahydro-8-ethyl-9-(N-benzoyl)pyrano[3,4-b]indole-1-acetic acid methyl ester was obtained in 66% yield by the reaction of methyl 1,8-dimethyl-1,3,4,9-tetrahydropyrano[3,4-b]indole-1-acetate (etodollic acid methyl ester) and benzoyl chloride.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.56-56
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• 1995

자연계에 널리 분포하고 있는 flavonoid 유도체들은 다양한 구조에 따라, 다양한 생물활성을 보인다. 최근에는 이들이 cyclooxygenase/lipoxygenase를 저해한다는 사실이 알려진 후에 이들 유도체들을 항염증제 또는 항알레르기 약물로 개발하려는 시도가 계속되고 있다. 이들 연구의 일환으로 본 연구자들은 여러 flavonoid유도체들에 대한 in vivo 항염증능 및 림프구증식억제능을 보고하였다 (Arch. Pharm. Res. 16, 18, 25 (1993), 17, 31, 236 (1994), Life Sci. 54, 313 (1994)). 또한 flavonoid 유도체들 중 apigenin-dimer인 수종의 biflavonoid들이 group II phospholipase $A_2$ 저해제인 것을 밝혔고 (BBRC 205, 843 (1994)), 이들 중 몇 종은 림프구증식능에 대하여 억제작용을 보인다는 것을 알았다 (Life Sci. in revision). 본 연구에서는 이들 biflavonoid 유도체들 중 amentoflavone과 ginkgetin을 중심으로 이들의 림프구증식억제능 및 in vivo에서의 항염증작용을 연구하였다. 그 결과, ginkgetin (1-10 $\mu$M)은 Con A와 LPS에 의해 유도되는 림프구중식을 비가역적으로 억제하였으며, 이들 유도체들은 마우스 귀부종에 대하여 복강내투여에서 강력한 항염증능을 보인다는 것을 알았다.

• Tuberculosis and Respiratory Diseases
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• v.56 no.5
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• pp.514-522
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• 2004

Background : Non-steroidal anti-inflammatory drugs (NSAID) are useful in chemoprevention of colorectal cancers. Continuous NSAID administation causes 40% to 50% reduction in relative risk for colorectal cancer. Sulindac possesses an antiproliferative effect and induces apoptosis and tumor regression on colon cancer and other types of cancers. We intended to analyze the effects of sulindac in three non-small cell lung cancer cell lines. Materials and Methods : The human lung cancer cell lines, A549, NCI-H157 and NCI-H460 were used for this study. Viability was tested by MTT assay, and cell death rate was measured by lactate dehydrogenase(LDH) release. Apoptosis was estimated by flow cytometric analysis and nuclear staining. Results: Sulindac was able to decrease the viability of non-small cell lung cancer cells in a dose- and time- dependent manner. In a parallel effect of sulindac on cell death rate, LDH release was increased in sulindac-treated lung cancer cells. Sulindac significantly increased apoptosis characterized by an increase of $sub-G_0/G_1$ fraction and morphological change of nuclei. The rate of apoptotic cells after sulindac treatment in lung cancer cells increased in a time- and dose- dependent manner in flow cytometric analysis. Apoptotic cells were defined as nuclear shrinkage, chromatin condensation and nuclear fragmentation of cells. Conclusion : Sulindac decreases viability and induces the apoptosis of lung cancer cells. Further studies will be needed to elucidate the potential mechanism of sulindac-induced apoptosis in lung cancer cells.

• The Korean Journal of Pharmacology
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• v.26 no.1
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• pp.51-54
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• 1990

Human leukocyte cathepsin-Gs are active participant in the active phase of inflammations like rheumatoid arthritis, emphysema and glomerular injury. Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for treatment of these inflammatory diseases. Mechanism of action of NSAIDs for treatment of inflammatory diseases, especially like rheumatoid arthritis, are known as the inhibitors of prostaglandin synthesis. Inhibitions of the activities of human leukocyte cathepsin-Gs by non-steroidal anti-inflammatory drugs, however, were not same as the known pharmacological effects (inhibition of cyclooxygenase) of these drugs. Among them, especially, sulindac, salicylate, phenylbutazone, oxyphenbutazone, and salicyluric acid inhibited human leukocyte cathepsin-Gs effectively. $IC_{50}s$ of each drug were 4.3mM, 14.3mM, 6.5mM, 11mM and 15mM respectively. The drugs which have same chemical structure and same degree of inhibition effect on cyclooxygenase showed different degree or no effect on inhibition of cathepsin G. These inhibition effect might be, beside of inhibition of cyclooxygenase in the prostaglandin synthesis pathway, another benefitial antiinflammatory effect of NSAIDs by direct protection against tissue destruction in inflammatory diseases.

• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.115-121
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• 1988

Although Saponin A from Panax ginseng has previously been shown to inhibit carageenin induced edema. a paucity of information exists on the effects of components from ginseng on the cellular inflammatory response. specifically polymorphonuclear leukocyte (PMNL) function. The purpose of this study was 10 determine the effects of isolated neutral dammarane saponins from ginseng (i.e..glycosidic derivatives of 20(S)-protopanaxadiol [ginsenoside $Rb_1,\;Rb_2$ and Rc] and 20(S)-protopanaxatriol [ginsenosides Re and $Rg_1$]) on in vivo PMNL function and to compare their effects with those produced by a steroidal anti-inflammatory agent (dexamethasone) and commercially available saponin. Dexamethasone. the ginsenosides and saponin were all shown to he potent inhibitors of PMNL chemotaxis using the $^{51}Cr$ assay with $5{\times}10^{-8}M$ f-met-leu-phe [FMLP] as the chemoattractant. Inhibition or PMNL chemotaxis by dexamethasone. the ginsenosides and saponin were all shown to be both time-and dose-dependent and these agents did not affect cellular viability at the concentrations tested Saponin and the ginsenosides were more potent inhibitors of chemotaxis than was dexamethasone. while oxidant generation (as measured by the luminol-enhaneed chemil-uminescence of PMNL using FMNL $[10^{-6}]$ as the stimulus) was inhibited by dexamethasone. the ginsenosides $(Rb_1\;Rb_2\;Rc\;Re\;and\;Rg_1)$ and saponin at a concentration of 1 ${\mu}M$ had no significant effect on PMNL chemiluminescence. Thus. the neutral dammarane saponins are potentially important modulators or PMNL function and their inhibitory effects may he differentiated from those of the Steroidal anti-inflammatory agents.

• Korean Journal of Oriental Medicine
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• v.6 no.1
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• pp.81-87
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• 2000

Chungpesagan-Tang (CST), a Korean traditional prescription composed of oriental medical herbs, has been used successfully to improve human health and regimen. This study was designed to examine the inhibitory effects of CST against in vitro ischemia/reperfusion-induced inflammatory response. We have characterized the production of prostaglandin $E_2$ and arachidonic acid during ischemia/reperfusion in the human neuroblastoma SK-N-MC and human monocytic macrophage U937 cells and the inhibitory effect of CST on these inflammation-related substance formation has been found out in this study. This result suggested that CST used in this experiment reinforced antiinflammatory potentials and protected cells against ischemia/reperfusion-induced inflammatory resopnse.

• Tuberculosis and Respiratory Diseases
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• v.41 no.6
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• pp.587-596
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• 1994

COPD의 치료에 대해 약술하였다. 예방을 위해서는 개인적으로는 금연, 국가사회적으로는 공해의 해결이 필요하며 진행된 질병에서는 진행을 막기 위한 감염의 예방 및 감염시 즉각적인 항균제 치료, 필요에 따라서 항염증제, 그리고 생활의 질을 높이기 위해서 각종 재활요법이 필요하다. 원활한 재활요법을 위해서는 필요한 기구 장비의 구입이 쉬워야 하고 치료진에서는 호흡기 전문의사, 호흡치료사, 의료기사, 병원 및 가정간호사, 사회사업가(social worker), 정신과의사, 영양사 등의 팀으로의 접근이 필요하고 제도적으로 보험적용이 되도록 해야 하겠다. 불구가 심한 예에서는 폐이식이 시도되며 기술적인 문제는 다소 해결된듯하나 장기공여자 등의 문제로 보편화되지는 않고 있다.