κ-卡拉胶协同三硝基苯磺酸致鼠结肠炎症的研究
PDF下载 (383)甄张赫 1,2,吴 玮 1,2,陈海敏 1,2 *.κ-卡拉胶协同三硝基苯磺酸致鼠结肠炎症的研究[J].宁波大学学报(理工版),2017,30(5):24-29.DOI:
ZHEN Zhang-he 1,2,WU Wei 1,2,CHEN Hai-min 1,2 *.Synergistic effects of κ-carrageenan on trinitrobenzene sulfonic acid induced intestinal inflammation in mice[J].Journal of Ningbo University(Natural Science & Engineering Edition),2017,30(5):24-29.DOI:
| Title: | Synergistic effects of κ-carrageenan on trinitrobenzene sulfonic acid induced intestinal inflammation in mice |
| 作者: | 甄张赫 1, 2, 吴 玮 1, 2, 陈海敏 1, 2 * |
| Author(s): | ZHEN Zhang-he 1, 2, WU Wei 1, 2, CHEN Hai-min 1, 2 * |
| 关键词: | κ-卡拉胶; 三硝基苯磺酸; 协同; 结肠炎; κ-carrageenan |
| Keywords: | trinitrobenzene sulfonic acid; synergy; intestinal inflammation |
| 分类号: | R285.5 |
| 文献标识码: | A |
| 摘要: | 为了研究κ-卡拉胶(CGN)协同加强三硝基苯磺酸(TNBS)对BALB/c小鼠结肠炎症的作用, 利用TNBS诱导BALB/c小鼠结肠炎模型, 分析了κ-卡拉胶处理后, 小鼠存活率及组织学变化, 随后应用表达谱芯片技术分析差异表达基因. 结果发现, κ-卡拉胶增加了TNBS诱导的小鼠死亡率及结肠损伤. 芯片数据发现: κ-卡拉胶协同TNBS处理后, 较之TNBS处理组出现619个变化基因, 部分炎症相关基因继续上调, 炎症应答程度出现增强. 而κ-卡拉胶单独处理不具有致炎性, 仅影响代谢系统等相关基因的变化. 表明κ-卡拉胶可通过增强上调炎症相关基因, 加重TNBS诱导小鼠结肠炎症反应. |
| Abstract: | This study attempts to investigate the synergistic effects of κ-carrageenan on trinitrobenzene sulfonic acid (TNBS)-induced BALB/c mice intestinal inflammation. BALB/c mice were treated with κ-carrageenan prior to administration of TNBS. The survival rate and histological changes of the colon tissue of mice were analyzed. The differentially expressed genes were analyzed by expression profile chip technology. The results indicated that TNBS-induced mortality and colonic damage were deteriorated by κ-carrageenan. Expression profile chip revealed that κ-carrageenan caused gene expression changes in metabolic pathways and other related pathways, but κ-carrageenanalone alone showed no proinflammatory effect. When mice were treated with TNBS, the significantly enriched pathways were closely related to inflammation. Compared to TNBS group, 619 genes were regulated in carrageenan+TNBS group. Some inflammation-related genes were further up-regulated. In summary, κ-carrageenan aggravated the TNBS-induced intestinal inflammation, which may be associated with the synergistical effects of κ-carrageenan on the enhancement of the TNBS via TLR4 pathway. |
| 参考文献 /References: | [1] COHEN S M, ITO N. A critical review of the toxicological effects of carrageenan and processed Eucheuma seaweed on the gastrointestinal tract[J]. Critical Reviews in Toxicology, 2002, 32(5):413-444. [2] GENEVA W H O. Safety evaluation of certain contaminants in food: Prepared by the sixty-fourth meeting of the joint FAO/WHO expert committee on food additives (JECFA)[EB/OL]. [2016-09-09]. http://xueshu.baidu. com/s?wd=Safety+evaluation+of+certain+contaminants+in+food%3A+Prepared+by+the+sixty-fourth+meeting+of+the+joint+FAO%2FWHO+expert+committee+on+food+additives+%28JECFA%29%5BEB%2FOL%5D&rsv_bp=0&tn=SE_baiduxueshu_c1gjeupa&rsv_spt=3&ie=utf-8&f=8&rsv_sug2=1&sc_f_para=sc_tasktype%3D%7BfirstSimpleSearch%7D&rsv_n=2. [3] WEINER M L. Food additive carrageenan Part II: A critical review of carrageenan in vivo safety studies[J]. Critical Reviews in Toxicology, 2014, 44(3):244-269. [4] KITSDKAWA Y, SAITO H, SUZUKI Y, et al. Effect of ingestion of eicosapentaenoic acid ethyl ester on carrageenan-induced colitis in guinea pigs[J]. Gastroenterology, 1992, 102(6):1859-1866. [5] BHATTACHARYYA S, GILL R, CHEN M L, et al. Toll-like receptor 4 mediates induction of the Bcl10- NFkappaB-interleukin-8 inflammatory pathway by carrageenan in human intestinal epithelial cells[J]. Biol Chem, 2008, 283(16):10550-10558. [6] BORTHAKUR A, BHATTACHARYYA S, DUDEJA P K, et al. Carrageenan induces interleukin-8 production through distinct Bcl10 pathway in normal human colonic epithelial cells[J]. Physiol Gastrointest Liver Physiol, 2007, 292(3):G829-G838. [7] BHATTACHARYYA S, XUE L, DEVKOTA S, et al. Carrageenan-induced colonic inflammation is reduced in Bcl10 null mice and increased in IL-10-deficient mice[EB/ OL]. [2016-09-09]. http://indigo.uic.edu/handle/10027/11172. [8] CHEN H M, WANG F, MAO H H, et al. Degraded lambda-carrageenan activates NF-kappaB and AP-1 pathways in macrophages and enhances LPS-induced TNF-alpha secretion through AP-1[J]. Biochim Biophys Acta, 1840, 7:2162-2170. [9] WU W, WANG F, GAO X, et al. Synergistic effect of κ-carrageenan on oxazolone-induced inflammation in BALB/c mice[J]. BMC Gastroenterol, 2016, 16(1):1-13. [10] WIRTZ S, NEURATH M F. Mouse models of inflammatory bowel disease[J]. Advances in Drug Delivery Review, 2007, 59:1073-1083. [11] MONDAL K, ROY I, GUPTA M N. κ-carrageenan as a carrier in affinity precipitation of yeast alcohol dehydrogenase[J]. Protein Expression and Purification, 2003, 32(1):151-160. [12] KING C D, RIOS G R, GREEN M D, et al. UDP- glucuronosyltransferases[J]. Current Drug Metabolism, 2000, 1(2):143-161. [13] ISHIKAWA M, SASAKI K, OZAKI M, et al. Inhibition of hepatic drug biotransformation by carrageenan- induced inflammation in the rat: Effect of sex hormone alterations[J]. Journal of Pharmacobio-Dynamics, 1992, 15(8):367-376. [14] BHATTACHARYYA S, GILL R, CHEN M L, et al. Toll-like receptor 4 mediates induction of the Bcl10- NFkappaB-interleukin-8 inflammatory pathway by carrageenan in human intestinal epithelial cells[J]. Journal of Biological Chemistry, 2008, 283:10550-10558. [15] BORTHAKUR A, BHATTACHATYYA S, DUDEJA P K, et al. Carrageenan induces interleukin-8 production through distinct Bcl10 pathway in normal human colonic epithelial cells[J]. American Journal of Physiology-Gastrointestinal and Liver Physiology, 2007, 292:G829-G838. [16] CHANDEL H S, PANDEY S P, SHUKLA D, et al. Toll- like receptors and CD40 modulate each other’s expression affecting Leishmania major infection[J]. Clinical & Experimental Immunology, 2014, 176(2):283-290. [17] FUKUI A, OHTA K, NISHI H, et al. Interleukin‐8 and CXCL10 expression in oral keratinocytes and fibroblasts via Toll‐like receptors[J]. Microbiology and Immunology, 2013, 57(3):198-206. [18] KURTH I, WILLIMANN K, SCHAERLI P, et al. Monocyte selectivity and tissue localization suggests a role for breast and kidney-expressed chemokine (BRAK) in macrophage development[J]. Journal of Experimental Medicine, 2001, 194(6):855-861. [19] STARNES T, RASILA K K, ROBERTSON M J, et al. The chemokine CXCL14 (BRAK) stimulates activated NK cell migration: Implications for the downregulation of CXCL14 in malignancy[J]. Experimental Hematology, 2006, 34(8):1101-1105. [20] NEMUNAITIS J. Macrophage function activating cytokines: Potential clinical application[J]. Critical Reviews in Oncology Hematology, 1993, 14(2):153-171. [21] FIXE P, PRALORAN V. Macrophage colony-stimulating- factor (M-CSF or CSF-1) and its receptor: Structure- function relationships[J]. European Cytokine Network, 1997, 8(2):125-136. |
| 备注/Memo: | 收稿日期: 2016－10－04. 宁波大学学报（理工版）网址: http://journallg.nbu.edu.cn/ 基金项目: 国家自然科学基金（81370532）. 第一作者: 甄张赫（1992－）, 女, 辽宁盖平人, 在读硕士研究生, 主要研究方向: 海洋药理. E-mail: 791633187@qq.com *通信作者: 陈海敏（1975－）, 女, 浙江瑞安人, 博士/研究员, 主要研究方向: 海洋药理. E-mail: chenhaimin@nbu.edu.cn 宁波大学学报（理工版）网址：http://journallg.nbu.edu.cn/ |
