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大脑α-促黑素的耗竭会改变大鼠体内前列腺素和白细胞介素引起的发热。

Depletion of brain alpha-MSH alters prostaglandin and interleukin fever in rats.

作者信息

Martin S M, Malkinson T J, Veale W L, Pittman Q J

机构信息

Biology Department, Mount Saint Vincent University Halifax, N.S., Canada.

出版信息

Brain Res. 1990 Sep 3;526(2):351-4. doi: 10.1016/0006-8993(90)91246-d.

Abstract

Alpha-melanocyte stimulating hormone (alpha-MSH), a putative endogenous antipyretic agent, is synthesized largely within neurons in the arcuate nucleus. To test the hypothesis that destruction of this area would increase the febrile response, male Wistar rats, treated as neonates with intraperitoneal injections of monosodium glutamate (MSG) or saline, were given intracerebroventricular (i.c.v.) injections of prostaglandin E1 (20 ng; 200 ng) or purified interleukin-1 (20 U) and body temperature was monitored. The fevers displayed by the MSG-treated animals were significantly greater (P less than 0.05) than those of the controls for the lower dose of PGE1 at 10-30 min and for IL-1 at 3-6 h after the injections. MSG-treated rats showed significant reduction (P less than 0.01) in alpha-MSH content of the medial basal hypothalamus and lateral septum when compared to saline controls. Body temperature response of non-febrile animals to high ambient temperature was not affected by the MSG treatment. These data support the hypothesis that alpha-MSH is an endogenous antipyretic in the rat.

摘要

α-黑素细胞刺激素(α-MSH)是一种假定的内源性解热剂,主要在弓状核的神经元内合成。为了验证破坏该区域会增强发热反应这一假说,将新生雄性Wistar大鼠腹腔注射谷氨酸单钠(MSG)或生理盐水进行处理,然后给它们脑室内注射前列腺素E1(20纳克;200纳克)或纯化的白细胞介素-1(20单位),并监测体温。在注射后10 - 30分钟,对于较低剂量的前列腺素E1,以及在3 - 6小时对于白细胞介素-1,MSG处理组动物的发热反应显著高于对照组(P小于0.05)。与生理盐水对照组相比,MSG处理组大鼠内侧基底下丘脑和外侧隔区的α-MSH含量显著降低(P小于0.01)。非发热动物对高温环境的体温反应不受MSG处理的影响。这些数据支持了α-MSH是大鼠内源性解热剂这一假说。

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