塞来昔布对脂多糖诱导的RAW264.7巨噬细胞炎症模型炎症因子的影响

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Abstract Objective To investigate the influence of Celecoxib on the secretion of inflammatory cytokines in RAW 264.7 macrophages model induced by lipopolysaccharide(LPS).Methods Mouse RAW 264.7 macrophage was cultured. 24 h after mouse RAW 264.7 macrophage was stimulated by LPS 1 μg/ml,then cell culture medium was collected.NO was tested by using Griess and the content of TNF-α and PGE2was tested by ELISA.Then the RAW 264.7 macrophage inflammation model was established.The toxic effect of celecoxib on LPS stimulated RAW 264.7 macrophages assayed by MTT.8.00 μmol/L Celecoxib was used to pretreat cell for 1 h,following of 1 μg/ml LPS added to stimulate cell for 24 h. Cell culture medium was collected to test the content of inflammatory factors NO,TNF-α and PGE2in culture medium. Results After 1 μg/ml of LPS stimulated RAW macrophages for 24 h,cell morphology changed obviously,the content of inflammatory factors NO,TNF-α and PGE2in culture medium were obvious higher than those of the control group(P＜0.01).Compared with DMSO control group,8.00 μmol/L Celecoxib group could significantly inhibit the release of inflammatory cytokines NO,TNF-α and PGE2induced by LPS in RAW 264.7 cells(P＜0.01).Conclusion Establishment of LPS induced macrophage model of RAW 264.7 and celecoxib can obvious inhibit the release of inflammatory cytokines NO,TNF-α and PGE2.

Key words： Celecoxib RAW 264.7 macrophage Lipopolysaccharide NO TNF-&alpha PGE2

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	PANG Yi-min
	GAN Lu
	WANG Xian-zhe
	SU Qi
	GUO Zhe
	HE Ping

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PANG Yi-min,GAN Lu,WANG Xian-zhe, et al. Influence of Celecoxib on inflammatory cytokines of inflammation model in RAW 264.7 macrophages induced by lipopolysaccharide[J]. 中国当代医药, 2017, 24(10): 4-7.

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	[参考文献]
[1]	刘俊田.动脉粥样硬化发病的炎症机制的研究进展[J].西安交通大学学报（医学版），2015，36（2）：141-152.
[2]	Galkina E，Ley K.Leukocyte influx in atherosclerosis[J].Curr Drug Targets，2007，8（12）：1239-1248.
[3]	吕田，叶海，张灿.安全性高的非甾体抗炎药的研究进展[J].中国新药杂志，2016，25（11）：1258-1265.
[4]	王宁，秦明照.选择性环氧化酶-2抑制剂与心血管事件风险[J].心血管病学进展，2013，34（2）：170-173.
[5]	Cannon CP，Cannon PJ.Physiology：COX-2 inhibitors and cardiovascular risk[J].Science，2012，336（6087）：1386-1387.
[6]	Warner TD，Mitchell JA.COX-2 selectivity alone does not define the cardiovascular risks associated with non-steroidal anti-inflammatory drugs[J].Lancet，2008，371（9608）：270-273.
[7]	毛近隆，李晓宇，孙蓉.环氧合酶（COX-2）抑制剂提高心血管安全性的抗炎机制探讨[J].中国中药杂志，2014，39（20）：4054-4059.
[8]	余功旺，黄文浩，刘爱梅，等.小鼠腹腔巨噬细胞炎症模型的建立[J].广东药学院学报，2014，30（6）：766-770.
[9]	阎雨，何阳阳，方莲花，等.巨噬细胞在动脉粥样硬化中的研究进展[J].中国药学杂志，2014，49（1）：7-10.
[10]	李玉秀，李覃，姬文婕，等.土荆皮乙酸对脂多糖诱导的RAW264.7巨噬细胞炎症反应及M1表型偏移的抑制作用[J].细胞与分子免疫学杂志，2016，32（5）：625-629.
[11]	Brune K，Patrignani P.New insights into the use of currently available non-steroidal anti-inflammatory drugs[J].J Pain Res，2015，8：105-118.
[12]	郭雨龙，刘爽.动脉粥样硬化的炎症因素：感染及自身免疫病[J].实用医学杂志，2016，32（10）：1713-1716.
[13]	黄波，陈畅.一氧化氮的功能及其作用机制（Ⅰ）——性质与功能[J].生物物理学报，2012，28（3）：173-184.
[14]	边宁，龚博君，郭军，等.一氧化氮/诱导型一氧化氮合酶在动脉粥样硬化过程中的作用[J].中国病理生理杂志，2014，30（3）：414-418.
[15]	郭远林，陈纪林.环氧化酶2与动脉粥样硬化：争议与前景[J].中华心血管病杂志，2006，34（1）：85-87.
[16]	Romero FI，Martínez-Calatrava MJ，Sánchez-Pernaute O，et al.Pharmacological modulation by celecoxib of cachexia associated with experimental arthritis and atherosclerosis in rabbits[J].Br J Pharmacol，2010，161（5）：1012-1022.
[17]	RavalM，FrankPG，Laury-KleintopL，etal.Celecoxibcombined with atorvastatin prevents progression of atherosclerosis[J]. J Surg Res，2010，163（2）：113-122.
[18]	Gitlin JM，Loftin CD.Cyclooxygenase-2 inhibition increases lipopolysaccharide-induced atherosclerosis in mice[J].Cardiovasc Res，2009，81（2）：400-407.