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作 者:陈庆德[1,2] 邓苏宏[1] 张璐思[1] 余晓芬[3] 胡四海[1]
机构地区:[1]南华大学病原生物学研究所,湖南421001 [2]郴州市妇幼保健院检验科,423000 [3]湘南学院微生物教研室,423000
出 处:《当代医学》2013年第26期27-29,共3页Contemporary Medicine
基 金:国家自然科学基金(81172890)
摘 要:目的观察P物质(substance P,SP)对脑膜炎奈瑟菌抗原诱导小胶质细胞表达环氧化酶2(cyclooxygenase-2,COX-2)和产生前列腺素E2(PGE2)的影响。方法原代培养小胶质细胞,根据不同的实验目的分为3组:(1)空白对照组:仅加入培养基;(2)脑膜炎奈瑟菌抗原组:加入10μg/mL抗原作用8 h;(3)SP组:在抗原刺激的同时加入1 nM SP作用8 h。采用RT-PCR检测小胶质细胞中COX-2的表达情况,ELISA检测培养上清中PGE2的产生。结果小胶质细胞未经任何处理情况下,COX-2表达量极少。当用10μg/mL脑膜炎奈瑟菌抗原处理8 h后,COX-2明显增高。而同时加用1 nM SP作用后,COX-2表达进一步增多。10μg/mL抗原作用8 h即可诱导一定水平的PGE2表达。而加用1 nM SP后,PGE2水平明显高于抗原组。此外,小胶质细胞经SP受体拮抗剂L-703606处理后,SP对COX-2的协同作用消失。结论 P物质能促进脑膜炎奈瑟菌诱导小胶质细胞表达COX-2及产生PGE2,从而可能加重中枢神经系统的炎症反应。Objective To observe the effect of SP on Neisseria meningitides-induced expression of cyclooxygenase-2(COX-2) and prostaglandin E 2 (PGE 2) production in microglial cells.Methods Depending on the purpose of the experiment, the microglial cells,which cultured primarily, weredivided into three groups: Control group: medium alone; Antigen group: added 10 Bg/mL Neisseria meningitidis for 8 h; SP group: With stimulating of antigen, 1 nM SP was added into culture medium for 8 h. The expression level of COX-2 in microglial cells was determined by RT-PCR, and ELISA was adopted for the detection of PEG 2 production in supematant. Results The expression of COX-2 in microglial cells was thimbleful without any treatment. After treatment of 10 p.g/mL Neisseria meningitides for 8 h, the level of COX-2 was significantly increased. However, after addition of 1 nM SP, the expression level of COX-2 was further increased. 10 }tg/mL Neissefia meningitides was able to induce the relative expression of PEG 2, and the level of PEG2 was significantly higher than that in the antigen group. In addition, after treatment of antagonist L-703606 for SP receptor, the synergy of SP against COX-2 was elimilated. Conclusion Substance P can promote Neisseria meningitidis induce microglial cells expression of COX-2 and production of PGE2, which may increase the inflammatory response of central nervous system.
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