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   cyclic adenosine monophosphate response element binding protein 的翻译结果: 查询用时:0.043秒
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cyclic
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Objective To investigate protein kinase A (PKA) signal regulatory mechanism of corticotropin-releasing hormone (CRH) mRNA expression, after CRH stimulated neuron of hypothalamic slices in rats in vitro. Methods After CRH stimulated corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro, the changes of activity of PKA signal pathway and their relationship with CRH mRNA expression were observed by reverse transcription-polymerase chain reaction (RT-PCR), Western...

Objective To investigate protein kinase A (PKA) signal regulatory mechanism of corticotropin-releasing hormone (CRH) mRNA expression, after CRH stimulated neuron of hypothalamic slices in rats in vitro. Methods After CRH stimulated corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro, the changes of activity of PKA signal pathway and their relationship with CRH mRNA expression were observed by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting. Results CRH may cause the remarkable increase in phosphorylated PKA (P-PKA), phosphorylated cyclic adenosine monophosphate response element-binding protein (P-CREB) and CRH mRNA content in hypothalamic slices in rats. However, CP-l54526 or H89 could have significant inhibition effects on the synthesis of P-PKA, P-CREB and CRH. Conclusion PKA signal pathway in ultrashort positive feedback control of CRH secretion in hypothalamus in the stress due to severe traumas.

目的 探讨大鼠下丘脑神经元表达促肾上腺皮质激素释放激素(CRH)mRNA的蛋白激酶A (PKA)信号调控机制。方法 通过大鼠下丘脑脑片实验模型,运用Westernblot及逆转录多聚合酶链反应(RT PCR)技术,观察CRH激活下丘脑促肾上腺皮质激素释放激素Ⅰ型受体(CRH1R)后PKA信号通路的活性变化,及其与CRHmRNA表达的关系。结果 CRH可引起下丘脑脑片磷酸化PKA、磷酸化环腺苷一磷酸反应元件结合蛋白(CREB)及CRHmRNA含量明显增加,而CP 15 45 2 6、H89可显著抑制磷酸化PKA、磷酸化CREB及CRHmRNA含量的增加。结论 在下丘脑离体脑片培养条件下,CRH可通过PKA途径实现对下丘脑神经元CRHmRNA的表达的超短正反馈调节。

Objective To investigate protein kinase A (PKA) signal regulatory mechanism of expression of corticotropin-releasing hormone (CRH) mRNA, after CRH stimulated neuron of hypothalamic slices in rats in vitro.Methods After CRH corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro was stimulated, the relation between the changes of activity of PKA signal pathway and those of CRH mRNA expression was observed by reverse transcription-polymerase chain reaction (RT-PCR)...

Objective To investigate protein kinase A (PKA) signal regulatory mechanism of expression of corticotropin-releasing hormone (CRH) mRNA, after CRH stimulated neuron of hypothalamic slices in rats in vitro.Methods After CRH corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro was stimulated, the relation between the changes of activity of PKA signal pathway and those of CRH mRNA expression was observed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting via the models of hypothalamic slices in rats.Results CRH may cause the remarkable increase in phosphorylated PKA (P-PKA), phosphorylated cyclic adenosine monophosphate response element-binding protein (P-CREB) and CRH mRNA content in hypothalamic slices in rats. However, CP-l54526 or H89 could have significant inhibitory effect on the synthesis of P-PKA, P-CREB and CRH.Conclusion PKA signal pathway in ultrashort positive feedback control of CRH secretion in hypothalamus in the stress is due to severe traumas.

目的 探讨大鼠下丘脑神经元表达促肾上腺皮质激素释放激素(CRH)mRNA的蛋白激酶A(PKA)信号调控机制。方法 通过大鼠下丘脑脑片实验模型,运用Westernblot及逆转录多聚合酶链反应(RT PCR)技术,观察CRH激活下丘脑促肾上腺皮质激素释放激素Ⅰ型受体(CRH1R)后PKA信号通路的活性变化,及其与CRHmRNA表达的关系。结果 CRH可引起下丘脑脑片磷酸化PKA、磷酸化环腺苷一磷酸反应元件结合蛋白(CREB)及CRHmRNA含量明显增加,而CP -154526、H89可显著抑制磷酸化PKA、磷酸化CREB及CRHmRNA含量的增加。结论 在严重创伤应激反应中, CRH主要通过PKA途径实现对下丘脑神经元CRHmRNA表达的超短正反馈调节。

OBJECTIVE:Intracellular signal transduction molecules including protein kinase C,protein kinase A,protein kinase G,mitogen activated protein kinase(MAPK),cyclic adenosine monophosphate response element binding protein(CREB),nuclear transcription factor kappa B(NF κ B) are involved in the initiation and maintenance of central sensitization of pathological pain.In this paper,we comprehend the characters of intracellular signal transduction so as to probe into the compliant alteration of initiation and transmission...

OBJECTIVE:Intracellular signal transduction molecules including protein kinase C,protein kinase A,protein kinase G,mitogen activated protein kinase(MAPK),cyclic adenosine monophosphate response element binding protein(CREB),nuclear transcription factor kappa B(NF κ B) are involved in the initiation and maintenance of central sensitization of pathological pain.In this paper,we comprehend the characters of intracellular signal transduction so as to probe into the compliant alteration of initiation and transmission of pain in central nervous system.DATA SOURCES:A computer based search for the articles related to intracellular signal transduction in central sensitization of pathological pain published between January 1997 and December 2004 were performed in Medline by using the key terms “ nociceptive,pain,sensitization,PKC,PKA,PKG,MAPK,ERK,JNK,CREB,NF kappa B" to retrieve and extract the articles in English.STUDY SELECTION:Over 400 articles were selected firstly.Inclusion criteria:① randomized controlled trials;② in vivo animals as experimental subjects;③ pathological pain models included injury induced inflammatory and nerve injury induced neuropathic pain.The literatures using non controlled trial,including defective experimental design and non pathological pain were excluded.DATA EXTRACTION:Over 80 articles were relevant to the intracellular signal transduction in central sensitization of pathological pain.Of the 80 articles,29 published in correlative and authoritative journals in the last 5 years were chosen.DATA SYNTHESIS:Nociceptive neuronal excitation of spinal dorsal horn was enhanced after tissue injury,which then induced central sensitization and leaded to noxious response of central nervous system to non noxious stimulation induced abnormal pain followed by promotion of stimulation response(hyperalgesia) to the injured area and non injury area surrounding the injured area.Central nervous system,altered with the initiation and transmission of pain compliantly,phosphorylated recipients and ion channels,promoted neuronal excitation of pain stimulation,altered gene expression,synthesized new protein to maintain the compliant changes of neurons.CONCLUSION:Many signal molecules participate in the process of central sensitization in nociceptive neurons.To study their mechanism can help to understand the initiation of pathological pain,and provide new ideas for clinical treatment of pathological pain.

目的:细胞内蛋白激酶C、蛋白激酶A、蛋白激酶G、丝裂原活化蛋白激酶、环磷酸腺苷反应元件结合蛋白、核转录因子κB等信号转导分子参与了病理性疼痛中枢敏感化的产生和持续过程,了解其特征,更有利于认识中枢神经系统在疼痛的产生与传递过程中发生的可塑性变化。资料来源:应用计算机检索Medlinel997-01/2004-12与病理性疼痛中枢敏感化细胞内信号转导相关文献,检索词“nociceptive,pain,sensi-tization,PKC,PKA,PKG,MAPK,ERK,JNK,CREB,NF-kappaB”等,分别进行检索并提炼,限定文献语言种类为英文。资料选择:就检索到的400余篇资料进行初审,纳入标准:①符合随机、对照条件。②以整体动物为实验研究对象。③包括炎症性疼痛和神经源性疼痛在内的病理性疼痛模型。排除没有对照组的文献、实验设计有缺陷的文献和非病理性疼痛的文献。资料提炼:共收集到80余篇关于病理性疼痛中枢敏感化与细胞内信号转导分子相关的文章。其中研究内容相似的,以近5年内发表在较权威杂志者优先。对符合标准的29篇文献进行分析。资料综合:组织损伤后,脊髓背角伤害感受性神经元兴奋性增强,产生中枢敏感化,导...

目的:细胞内蛋白激酶C、蛋白激酶A、蛋白激酶G、丝裂原活化蛋白激酶、环磷酸腺苷反应元件结合蛋白、核转录因子κB等信号转导分子参与了病理性疼痛中枢敏感化的产生和持续过程,了解其特征,更有利于认识中枢神经系统在疼痛的产生与传递过程中发生的可塑性变化。资料来源:应用计算机检索Medlinel997-01/2004-12与病理性疼痛中枢敏感化细胞内信号转导相关文献,检索词“nociceptive,pain,sensi-tization,PKC,PKA,PKG,MAPK,ERK,JNK,CREB,NF-kappaB”等,分别进行检索并提炼,限定文献语言种类为英文。资料选择:就检索到的400余篇资料进行初审,纳入标准:①符合随机、对照条件。②以整体动物为实验研究对象。③包括炎症性疼痛和神经源性疼痛在内的病理性疼痛模型。排除没有对照组的文献、实验设计有缺陷的文献和非病理性疼痛的文献。资料提炼:共收集到80余篇关于病理性疼痛中枢敏感化与细胞内信号转导分子相关的文章。其中研究内容相似的,以近5年内发表在较权威杂志者优先。对符合标准的29篇文献进行分析。资料综合:组织损伤后,脊髓背角伤害感受性神经元兴奋性增强,产生中枢敏感化,导致中枢神经系统对非伤害性刺激产生疼痛异常的伤害性反应,对伤害区域内和伤害区域周围非伤害区域的刺激反应增强(痛觉过敏)。中枢?

 

 


 

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