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急性抗阻运动通过激活大鼠体内的内源性大麻素系统诱导产生抗伤害感受作用。

Acute resistance exercise induces antinociception by activation of the endocannabinoid system in rats.

作者信息

Galdino Giovane, Romero Thiago, Pinho da Silva José Felippe, Aguiar Daniele, de Paula Ana Maria, Cruz Jader, Parrella Cosimo, Piscitelli Fabiana, Duarte Igor, Di Marzo Vincenzo, Perez Andrea

机构信息

From the Department of Pharmacology, Department of Physiology, Institute of Biological Sciences, Department of Physics, and Department of Biochemistry, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil; and Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Pozzuoli, Napoli, Italy.

出版信息

Anesth Analg. 2014 Sep;119(3):702-715. doi: 10.1213/ANE.0000000000000340.

Abstract

BACKGROUND

Resistance exercise (RE) is also known as strength training, and it is performed to increase the strength and mass of muscles, bone strength, and metabolism. RE has been increasingly prescribed for pain relief. However, the endogenous mechanisms underlying this antinociceptive effect are still largely unexplored. Thus, we investigated the involvement of the endocannabinoid system in RE-induced antinociception.

METHODS

Male Wistar rats were submitted to acute RE in a weight-lifting model. The nociceptive threshold was measured by a mechanical nociceptive test (paw pressure) before and after exercise. To investigate the involvement of cannabinoid receptors and endocannabinoids in RE-induced antinociception, cannabinoid receptor inverse agonists, endocannabinoid metabolizing enzyme inhibitors, and an anandamide reuptake inhibitor were injected before RE. After RE, CB1 cannabinoid receptors were quantified in rat brain tissue by Western blot and immunofluorescence. In addition, endocannabinoid plasma levels were measured by isotope dilution-liquid chromatography mass spectrometry.

RESULTS

RE-induced antinociception was prevented by preinjection with CB1 and CB2 cannabinoid receptor inverse agonists. By contrast, preadministration of metabolizing enzyme inhibitors and the anandamide reuptake inhibitor prolonged and enhanced this effect. RE also produced an increase in the expression and activation of CB1 cannabinoid receptors in rat brain tissue and in the dorsolateral and ventrolateral periaqueductal regions and an increase in endocannabinoid plasma levels.

CONCLUSIONS

The present study suggests that a single session of RE activates the endocannabinoid system to induce antinociception.

摘要

背景

抗阻运动(RE)也被称为力量训练,其目的是增加肌肉力量和质量、骨骼强度以及新陈代谢。越来越多的研究表明,抗阻运动可用于缓解疼痛。然而,这种镇痛作用的内在机制在很大程度上仍未得到充分探索。因此,我们研究了内源性大麻素系统在抗阻运动诱导的镇痛中的作用。

方法

将雄性Wistar大鼠置于举重模型中进行急性抗阻运动。在运动前后通过机械性伤害感受测试(爪部压力)测量伤害感受阈值。为了研究大麻素受体和内源性大麻素在抗阻运动诱导的镇痛中的作用,在抗阻运动前注射大麻素受体反向激动剂、内源性大麻素代谢酶抑制剂和花生四烯乙醇胺再摄取抑制剂。抗阻运动后,通过蛋白质免疫印迹法和免疫荧光法对大鼠脑组织中的CB1大麻素受体进行定量分析。此外,通过同位素稀释-液相色谱质谱法测量内源性大麻素的血浆水平。

结果

预先注射CB1和CB2大麻素受体反向激动剂可阻止抗阻运动诱导的镇痛作用。相比之下,预先给予代谢酶抑制剂和花生四烯乙醇胺再摄取抑制剂可延长并增强这种作用。抗阻运动还使大鼠脑组织以及背外侧和腹外侧导水管周围区域的CB1大麻素受体表达和激活增加,内源性大麻素血浆水平升高。

结论

本研究表明,单次抗阻运动可激活内源性大麻素系统以诱导镇痛。

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