首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >The effect of protein kinase C-delta knockdown on anti-free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine-treated rats.
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The effect of protein kinase C-delta knockdown on anti-free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine-treated rats.

机译:蛋白激酶C-δ敲低对苯丙醇胺治疗的大鼠抗自由基酶和神经肽Y基因表达的影响。

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摘要

Hypothalamic neuropeptide Y (NPY) has been reported to involve in regulating behavioral response of phenylpropanolamine (PPA), a sympathomimetic agent. This study explored if protein kinase C (PKC)-delta signaling participated in this regulation. Moreover, possible roles of anti-free radical enzyme catalase (CAT) and nitrogen oxide synthase (NOS) were also examined. Rats were treated daily with PPA for 4 days. Changes in food intake and hypothalamic NPY, PKCdelta, CAT, and NOS contents were assessed and compared. Results showed that PKCdelta and CAT increased during PPA treatment, which were concomitant with decreases in NPY content and food intake, while the change of NOS was expressed differently. Moreover, PKCdelta knockdown could modify PPA anorexia as well as NPY and CAT expression, while NOS expression remained unchanged. Furthermore, pre-treatment with NOS inhibitor could modify both PPA anorexia and NPY content. It is suggested that PKCdelta participates in the anorectic response of PPA via the modulation of NPY and CAT, while NOS contribute to this modulation via a different mechanism during PPA treatment. Results provide molecular mechanism of NPY-mediated PPA anorexia and may aid the therapeutic research of PPA and other anti-obesity drugs.
机译:下丘脑神经肽Y(NPY)已报道参与调节拟交感神经药苯丙醇胺(PPA)的行为反应。这项研究探讨了蛋白激酶C(PKC)-δ信号传导是否参与了这一调控。此外,还研究了抗自由基酶过氧化氢酶(CAT)和氮氧化物合酶(NOS)的可能作用。每天用PPA处理大鼠4天。评估并比较食物摄入量和下丘脑NPY,PKCdelta,CAT和NOS含量的变化。结果表明,PPA处理期间PKCdelta和CAT升高,这与NPY含量和食物摄入减少有关,而NOS的表达则有所不同。此外,PKCdelta敲除可以修改PPA厌食症以及NPY和CAT表达,而NOS表达保持不变。此外,用NOS抑制剂进行预处理可以同时改变PPA厌食症和NPY含量。提示PKCdelta通过NPY和CAT的调节参与PPA的厌食反应,而NOS在PPA治疗期间通过不同的机制参与这种调节。研究结果提供了NPY介导的PPA厌食症的分子机制,可能有助于PPA和其他抗肥胖药的治疗研究。

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