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沃克256荷瘤大鼠厌食症中强啡肽A耗竭的评估。

Assessment of dynorphin-A depletion in the anorexia of Walker-256 tumor bearing rats.

作者信息

Yim G K, Bryant H U, Malven P V

出版信息

Physiol Behav. 1985 Jul;35(1):117-20. doi: 10.1016/0031-9384(85)90182-9.

Abstract

Rats bearing the Walker-256 (W-256) tumor display an anorexic profile which resembles that of normal animals forced to drink 2% NaCl [2,24], a regimen which depletes neurohypophyseal dynorphin-A (DYN) [3,9]. As expected, the naloxone reversible feeding induced by 2-deoxy-D-glucose (2-DG) was attenuated (36%) in the W-256 tumor bearing rats (TBR). Interestingly, immunoreactive (ir) levels of dynorphin-A 1-17 (DYN-17) and its postulated breakdown product, dynorphin-A 1-18 (DYN-8), were also reduced in the neurohypophysis of W-256 TBR by 42 and 50%, respectively. However, ir-DYN levels were not reduced in TBR in those brain regions which are probably involved in the regulation of appetite (e.g., hypothalamus). 2-DG itself did not consistently affect ir-DYN levels in any tissue for either controls or TBR. The ratio of DYN-8 to DYN-17 did not change in response to any treatment, including the depletion of both peptides from the NIL of TBR. In summary, the present data do not support DYN depletion as being a factor which contributes to the anorexia of the W-256 TBR.

摘要

携带Walker-256(W-256)肿瘤的大鼠表现出一种厌食症状,类似于被迫饮用2%氯化钠的正常动物的症状[2,24],这种饮食方案会消耗神经垂体强啡肽-A(DYN)[3,9]。正如预期的那样,2-脱氧-D-葡萄糖(2-DG)诱导的纳洛酮可逆性进食在携带W-256肿瘤的大鼠(TBR)中减弱了(36%)。有趣的是,强啡肽-A 1-17(DYN-17)及其假定的分解产物强啡肽-A 1-18(DYN-8)的免疫反应性(ir)水平在W-256 TBR的神经垂体中也分别降低了42%和50%。然而,在可能参与食欲调节的脑区(如下丘脑),TBR中的ir-DYN水平并未降低。2-DG本身对对照组或TBR的任何组织中的ir-DYN水平均无一致影响。DYN-8与DYN-17的比值对任何处理均无变化,包括从TBR的神经垂体中耗尽这两种肽。总之,目前的数据不支持DYN耗尽是导致W-256 TBR厌食的一个因素。

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