本实验旨在探讨奶牛输卵管上皮细胞中是否存在前列腺素E2受体EP2和EP4,且该受体mRNA表达是否受雌激素(E2)的调控。将前列腺素类化合物PGE2和受体选择性激动剂(butaprost)按10-9mol/L-10-5mol/L的浓度分别作用于体外培养的奶牛输卵管上...本实验旨在探讨奶牛输卵管上皮细胞中是否存在前列腺素E2受体EP2和EP4,且该受体mRNA表达是否受雌激素(E2)的调控。将前列腺素类化合物PGE2和受体选择性激动剂(butaprost)按10-9mol/L-10-5mol/L的浓度分别作用于体外培养的奶牛输卵管上皮细胞,应用Elisa方法检测细胞中第二信使cAMP量的变化。然后,将E2作用于体外培养的奶牛输卵管上皮细胞,应用real time RT-PCR技术检测EP2和EP4受体mRNA表达量的变化。Elisa实验结果显示,前列腺素类化合物PGE2和受体选择性激动剂(butaprost)可引起奶牛输卵管上皮中cAMP量的变化,且cAMP量具有对PGE2和butaprost浓度依存性的变化规律,表明奶牛输卵管上皮细胞中存在前列腺素受体EP2和EP4。Real time RT-PCR实验结果表明,奶牛输卵管上皮细胞中存在前列腺素受体EP2和EP4,且E2对EP2和EP4受体mRNA的表达具有调控作用,低浓度(10-12mol/L)可提高该受体mRNA的表达量。展开更多
Fever is an adaptive host response coordinated by the central nervous system （CNS） during systemic immune challenge. Recent research shed light on the mechanism of fever generation, particularly the underlying neura...Fever is an adaptive host response coordinated by the central nervous system （CNS） during systemic immune challenge. Recent research shed light on the mechanism of fever generation, particularly the underlying neural pathways. In this review, we first briefly summarize current views on the mechanism of sensing microbial infection by the nervous system, and the roles of prostaglandin E2 （PGE2） and its receptors in fever; then we focus on the neural circuits underlying fever generation, particularly their relationship with the distribution of PGE2 receptors within the CNS. At the end, an overall neurochemical model of fever generation is presented, pointing to the direction for future studies.展开更多
文摘本实验旨在探讨奶牛输卵管上皮细胞中是否存在前列腺素E2受体EP2和EP4,且该受体mRNA表达是否受雌激素(E2)的调控。将前列腺素类化合物PGE2和受体选择性激动剂(butaprost)按10-9mol/L-10-5mol/L的浓度分别作用于体外培养的奶牛输卵管上皮细胞,应用Elisa方法检测细胞中第二信使cAMP量的变化。然后,将E2作用于体外培养的奶牛输卵管上皮细胞,应用real time RT-PCR技术检测EP2和EP4受体mRNA表达量的变化。Elisa实验结果显示,前列腺素类化合物PGE2和受体选择性激动剂(butaprost)可引起奶牛输卵管上皮中cAMP量的变化,且cAMP量具有对PGE2和butaprost浓度依存性的变化规律,表明奶牛输卵管上皮细胞中存在前列腺素受体EP2和EP4。Real time RT-PCR实验结果表明,奶牛输卵管上皮细胞中存在前列腺素受体EP2和EP4,且E2对EP2和EP4受体mRNA的表达具有调控作用,低浓度(10-12mol/L)可提高该受体mRNA的表达量。
文摘Fever is an adaptive host response coordinated by the central nervous system （CNS） during systemic immune challenge. Recent research shed light on the mechanism of fever generation, particularly the underlying neural pathways. In this review, we first briefly summarize current views on the mechanism of sensing microbial infection by the nervous system, and the roles of prostaglandin E2 （PGE2） and its receptors in fever; then we focus on the neural circuits underlying fever generation, particularly their relationship with the distribution of PGE2 receptors within the CNS. At the end, an overall neurochemical model of fever generation is presented, pointing to the direction for future studies.
