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.