期刊文献+

SO_2吸入对大鼠海马组织炎性因子水平、钙稳态和即早基因表达的影响 被引量:4

SO_2 inhalation-induced effects on cytokine level,intracellular Ca^(2+) content and the expression of immediate earlygene in rat hippocampus
下载PDF
导出
摘要 采用动式熏气法研究了不同浓度SO2(7、14、28和56mg.m-3)吸入对大鼠海马组织炎性因子白介素-1β(Interleukin-1β,Il-1β)、肿瘤坏死因子(Tumor Necrosis Factor-α,TNF-α)水平、神经元胞内游离Ca2+浓度以及即早基因c-fos和c-jun mRNA表达的影响.结果表明:SO2可造成海马组织Il-1β(p<0.01)和TNF-α(p<0.05)水平显著增高,但低浓度下(7、14mg.m-3)作用较为明显;SO2可显著增加神经元胞内钙离子浓度,上调c-fos和c-jun mRNA的表达,且呈现出明显的剂量-效应关系.这一结果从整体水平上说明了SO2对中枢神经系统的损伤效应,并提示其可能的分子机制与炎性反应、钙离子稳态及即早基因表达相关. SO2 inhalation-induced effects on the levels of interleukin-1β(Il-1β)and tumor necrosis factor-α(TNF-α),intracellular Ca^2+ content,and the expression of immediate earlygene(c-fos and c-jun)in rat hippocampus were studied by treating Wistar rats with SO2 at various concentrations(7,14,28 and 56 mg·m^-3).The results indicate that SO2 inhalation significantly increased the levels of Il-1β(p〈0.01)and TNF-α(p〈0.05),and the effect was obvious after lower concentration exposure(7 and 14 mg·m-3).Also,SO2 significantly elevated the content of intracellular Ca^2+,and up-regulated the expression of c-fos and c-jun mRNA in a concentration-dependent manner.The results imply that SO2 inhalation could cause injury to the central neuronal system,and suggest that the molecular mechanisms might be involved in inflammation,intracellular calcium balance,and the expression of immediate earlygene.
出处 《环境科学学报》 CAS CSCD 北大核心 2008年第11期2315-2320,共6页 Acta Scientiae Circumstantiae
基金 国家自然科学基金资助项目(No.20607013 20877050) 山西省青年科学基金资助项目(No.20051043) 山西省回国留学人员科研项目 山西省高等学校优秀青年学术带头人支持计划资助~~
关键词 SO2 海马神经元 白细胞介素-1β(Il-1β) 肿瘤坏死因子(TNF-α) 胞内Ca2+水平 即早基因 SO2, hippocampus, interleukin-1β(Il-1β), tumor necrosis factor-α(TNF-α), intracellular Ca2+, immediate earlygene
  • 相关文献

二级参考文献17

  • 1[2]Dai XQ(戴晓晴).Effects of lead on sodium current and potassium current in adult rat dorsal root ganglion.Hygiene Res(卫生研究),1998,27: 32~35 ( Chinese,English abstract).
  • 2[3]Calabresi P,Pisani A,Mercuri NB,Bemardi G.On the mechanisms underlying hypoxia-induced membrane depolarization in striatal neurons.Brain,1995,118:1027 ~1038.
  • 3[4]Krnjevic K,Leblond J.Changes in membrane currents of hippocampal neurons evoked by brief anoxia.J Neurophysiol,1989,62:15~30.
  • 4[5]Urenjak J,Obrenovitch TP.Pharmacological modulation of voltage-gated Na+ channels: a rational and effective strategy against isehemic brain damage.Pharmacol Rev,1996,48:21~67.
  • 5[6]Taylor CP,Meldrum BS.Na + channels as targets for neuroproteetive drugs.Trends Pharmacol Sci,1995,16:309 ~316.
  • 6[7]Shapiro R.Genetic effects of bisulfite ( sulfur dioxide).Mutat Res,1977,38:149~176.
  • 7[8]Meng ZQ,Zhang LZ.Cytogenetie damage induced in human lymphocytes by sodium bisulfite.Mutat Res,1992,298: 63~69.
  • 8[9]Meng ZQ,Zhang B.Polymerase chain reaction-based deletion screening of bisultite ( sulfur dioxide ) -enhanced gpt-mutants in CHO-AS52 cells.Mutat Res,1999,425:81~85.
  • 9[10]Zou BD,Chen YZ,Wu CH,Zhou PA.Blockade of US0488H on sodium currents in acutely isolated mice hippocampal CA3 pyramidal neurons.Brain Res,2000,855:132~136.
  • 10[11]Boening JA,Kass IS,Cottrcll JE,Chambers G.The effect of blocking sodium influx on anoxie damage in the rat hippocampal slice.Neuroseienee,1989,33:263~268.

共引文献35

同被引文献51

  • 1李怡,朱彤.大气颗粒物致机体损伤的OH自由基机制[J].生态毒理学报,2007,2(2):142-149. 被引量:11
  • 2Hong YC, Lee JT, Kim H, Ha EH, Schwartz J, Christiani DC. Effects of air pollutants on acute stroke mortality [J]. Environ Health Perspect, 2002, 110 (2): 187-191.
  • 3Kampaa M, Castanas E. Human health effects of air pollution [J]. Environ Pollut, 2008, 151 (2): 362-367.
  • 4Szyszkowicz M, Rowe BH, Kaplan GG. Ambient sulphur dioxide exposure and emergency department visits for migraine in Vancouver, Canada [J]. lnt J Occup Med Environ Health, 2009, 22 (1): 7-12.
  • 5Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression [J]. Trends lmmunol, 2006, 27 (1): 24-31.
  • 6Sama P, Long TC, Hester S, Tajuba J, Parker J, Chen LC, Veronesi B. The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter [J]. Inhal Toxicol, 2007, 19 (13): 1079-1087.
  • 7Calderon-Garciduenas L, Reed W, Maronpot RR, Henriquez-Roldan C, Delgado-Chavez R, Calderon-Garciduenas A, Dragustinovis I, Franco- Lira M, Aragon-Flores M, Solt AC, Altenburg M, Torres-Jardon R, Swenberg JA. Brain inflammation and Alzheimer's-like pathology in individuals exposed to severe air pollution [J]. Toxicol Pathol, 2004, 32 (6): 650-658.
  • 8Calderon-Garciduenas L, Solt AC, Henriquez-Roldan C, Torres-Jardon R, Nuse B, Herritt L, Villarreal-Calder6n R, Osnaya N, Stone I, Garcia R, Brooks DM, Gonzatlez-Maciel A, Reynoso-Robles R, Delgado- Chavez R, Reed W. Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults [J]. ToxicolPathol, 2008, 36 (2): 289-310.
  • 9Clark IA, Alleva LM, Vissel B. The roles of TNF in brain dysfunction and disease [J]. Pharmacol Ther, 2010, 128 (3): 519-548.
  • 10Sang N, Yun Y, Li HY, Hou L, Han M, Li GK. SO2 inhalation contributes to the development and progression of ischemic stroke in the brain [J]. Toxicol Sci, 2010, 114 (2): 226-236.

引证文献4

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部