[1]张广芹,马梦娇,于晓璐,等.143抑制LPS诱导的细胞炎症反应[J].南京师范大学学报(自然科学版),2019,42(01):95.[doi:10.3969/j.issn.1001-4616.2019.01.015]
　Zhang Guangqin,Ma Mengjiao,Yu Xiaolu,et al.The Inhibitory Effect of 143 on LPS-InducedCellular Inflammatory Response[J].Journal of Nanjing Normal University(Natural Science Edition),2019,42(01):95.[doi:10.3969/j.issn.1001-4616.2019.01.015]
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143抑制LPS诱导的细胞炎症反应()
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《南京师范大学学报》（自然科学版）[ISSN:1001-4616/CN:32-1239/N]

卷:
第42卷
期数:
2019年01期
页码:
95
栏目:
·生命科学·
出版日期:
2019-03-20

文章信息/Info

Title:
The Inhibitory Effect of 143 on LPS-InducedCellular Inflammatory Response
文章编号:
1001-4616(2019)01-0095-07
作者:
张广芹; 马梦娇; 于晓璐; 温传俊
南京师范大学生命科学学院,分子细胞生物学研究所,江苏 南京 210023
Author(s):
Zhang Guangqin; Ma Mengjiao; Yu Xiaolu; Wen Chuanjun
School of Life Sciences,Nanjing Normal University,Institute of Molecular and Cell Biology,Nanjing 210023,China
关键词:
143; 炎症反应; iNOS; COX-2; NF-κB
Keywords:
143; inflammatory response; iNOS; COX-2; NF-kB
分类号:
Q291
DOI:
10.3969/j.issn.1001-4616.2019.01.015
文献标志码:
A
摘要:
机体异常炎症反应与各种疾病的发生息息相关. 实验室通过前期工作,筛选出抗炎效果较好的化合物,并将其命名为143. 通过LPS诱导RAW264.7细胞和BV2细胞作为炎症细胞模型,用不同浓度的143处理细胞,观察其抗炎效应. 用MTS检测不同浓度143对细胞活力的影响,NO试剂盒检测细胞培养上清NO含量的变化,Western blot检测NF-κB p-p65、iNOS、COX-2蛋白的表达情况. 结果显示,143在浓度小于10 μmol/L时对两种细胞活力没有影响; 143在浓度为10 μmol/L时能显著抑制细胞上清中NO的含量,并显著抑制细胞中炎症相关蛋白因子NF-κB p-p65、iNOS、COX-2的表达.
Abstract:
Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. We have previously screened a compound,named as 143,with efficient anti-inflammatory effects. The present study aimed to examine its effects based on LPS-induced inflammatory cell models in RAW264.7 and BV2 cells. MTS was used to detect the effect of different concentrations of 143 on cell viability. The NO kit was used to detect the change of NO content in cell culture supernatant. The expression of NF-kB p-p65,iNOS and COX-2 protein was detected by Western blot. The results showed that 10 μmol/L 143 had no effect on the cell viability but significantly inhibited the release of NO in LPS-stimulated cells. In addition,143 significantly inhibited the expression of inflammation-related protein factors,such as NF-kB p-p65,iNOS,COX-in LPS-stimulated cells.

参考文献/References:

[1] NK R,S B,SK V,et al. Frontline science:aspirin-triggered resolvin D1 controls herpes simplex virus-induced corneal immunopathology[J]. Journal of leukocyte biology,2017,102(5):jlb.3HI1216-511RR.
[2]王菊勇,胡兵,徐振晔,等. NF-кB/iNOS-COX-2信号转导通路与肺癌[J]. 肿瘤防治研究,2009,36(4):342-345.
[3]ATCHISON M L,PERRY R P. The role of the kappa enhancer and its binding factor NF-kappa B in the developmental regulation of kappa gene transcription[J]. Cell,1987,48(1):121.
[4]周峰,刘子杰,段勇. 炎症在肿瘤发生过程中所起作用研究进展[J]. 世界最新医学信息文摘,2018(9):84-85.
[5]IM N.Inflammation and cancer[J]. Nature,2002,420(6917):860-867.
[6]TERRANDO N,MONACO C,MA D,et al. Tumor necrosis factor-α triggers a cytokine cascade yielding postoperative cognitive decline[J]. Proceedings of the national academy of sciences of the United States of America,2010,107(47):20518-20522.
[7]GHOSH S,KARIN M. Missing pieces in the NF-kappaB puzzle[J]. Cell,2002,109(4):S81-S96.
[8]RASK K,ZHU Y,WANG W,et al. Ovarian epithelial cancer:a role for PGE2-synthesis and signalling in malignant transformation and progression[J]. Molecular cancer,2006,5(1):62.
[9]VACAS S,DEGOS V,TRACEY K J,et al. High-mobility group box 1 protein initiates postoperative cognitive decline by engaging bone marrow-derived macrophages[J]. Anesthesiology,2014,120(5):1160.
[10]YAMAMOTO K,ARAKAWA T,UEDA N,et al. Transcriptional roles of nuclear factor kappa B and nuclear factor-interleukin-6 in the tumor necrosis factor alpha-dependent induction of cyclooxygenase-2 in MC3T3-E1 cells[J]. Journal of biological chemistry,1995,270(52):31315-31320.
[11]吴念江,吴立新,吴忆宁. 咪唑斯汀的临床应用新进展[J]. 西北药学杂志,2009,24(1):80-80.
[12]成兰. 咪唑斯汀的临床应用[J]. 临床医学,2002,22(4):56-56.
[13]陈启信,沈卫峰,罗邦尧. 左旋咪唑治疗类风湿性关节炎[J]. 国外医学参考资料:内科学分册,1978(2):25.
[14]XIONG H,CHENG Y,ZHANG X,et al. Effects of taraxasterol on iNOS and COX-2 expression in LPS-induced RAW 264.7 macrophages[J]. Journal of ethnopharmacology,2014,155(1):753-757.
[15]KARIN M,GRETEN F R. NF-kappaB:linking inflammation and immunity to cancer development and progression[J]. Nature reviews immunology,2005,5(10):749-759.
[16]尹兆宝,吴洪梅,林松华,等. 炎症与阿尔茨海默病[J]. 国际老年医学杂志,1998(6):247-250.
[17]SARGSYAN S A,THURMAN J M. Molecular imaging of autoimmune diseases and inflammation[J]. Molecular imaging,2012,11(3):251-264.
[18]PARK S W,LEE S G,SONG S H,et al. The effect of nitric oxide on cyclooxygenase-2(COX-2)overexpression in head and neck cancer cell lines[J]. International journal of cancer,2010,107(5):729-738.
[19]ESCáRCEGA R O,FUENTES A S,GARCíA C M,et al. The transcription factor nuclear factor-Kappa B and cancer[J]. Clinical oncology,2007,19(2):154-161.
[20]KIM J B,HAN A R,PARK E Y,et al. Inhibition of LPS-induced iNOS,COX-2 and cytokines expression by poncirin through the NF-kappaB inactivation in RAW 264.7 macrophage cells[J]. Biological & pharmaceutical bulletin,2007,30(12):2345-2351.
[21]VACAS S,DEGOS V,TRACEY K J,et al. High-mobility group box 1 protein initiates postoperative cognitive decline by engaging bone marrow-derived macrophages[J]. Anesthesiology,2014,120(5):1160.
[22]WANG D,DUBOIS R N. The role of COX-2 in intestinal inflammation and colorectal cancer[J]. Oncogene,2010,29(6):781.
[23]XU Y,WANG C,WU L,et al. Comparison of inhibitory effects of nine flavonoids on prostaglandin E2 production and COX-2 expression in LPS-stimulated RAW264.7 macrophages[C]//International Conference on Biomedical Engineering and Biotechnology. Macao:ICBEB,2012:981-984.
[24]MCGEER P L,ITAGAKI S,BOYES B E,et al. Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson’s and Alzheimer’s disease brains[J]. Neurology,1988,38(8):1285. [责任编辑:黄 敏]

备注/Memo

备注/Memo:
收稿日期:2018-06-20.
基金项目:国家自然科学基金(2012104GZ30057).
通讯联系人:温传俊,副教授,研究方向:肿瘤分子细胞生物学. E-mail:wenchuanjun@hotmail.com
更新日期/Last Update: 2019-03-30