Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran.
Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran; Laboratory of Molecular Neuroscience, Kerman Neuroscience Research Center (KNRC), Kerman University of Medical Sciences, Kerman, Iran.
Eur J Pharmacol. 2018 Aug 5;832:75-80. doi: 10.1016/j.ejphar.2018.05.013. Epub 2018 May 17.
The phytohormone abscisic acid exists in animal tissues particularly in the brain. However, its neurophysiological effects have not yet been fully clarified. This study was designed to evaluate the possible antinociceptive effects of abscisic acid on animal models of pain and determine its possible signaling mechanism. Tail-flick, hot-plate and formalin tests were used to assess the nociceptive threshold. All experiments were carried out on male Wistar rats. To determine the role of Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) and opioid receptors on the induction of abscisic acid antinociception, specific antagonists were injected 15 min before abscisic acid. The data showed that abscisic acid (5, 10 and 15 µg/rat, i.c.v.) significantly decreased pain responses in formalin test. In addition, it could also produce dose-dependent antinociceptive effect in tail-flick and hot-plate tests. Administration of PPARβ/δ antagonist (GSK0660, 80 nM, i.c.v.) significantly attenuated the antinociceptive effect of abscisic acid in all tests. The antinociceptive effects of abscisic acid were completely inhibited by naloxone (6 µg, i.c.v.) during the time course of tail-flick and hot-plate tests. The results indicated that the central injection of abscisic acid has potent pain-relieving property which is mediated partly via the PPAR β/δ and opioid signaling.
植物激素脱落酸存在于动物组织中,特别是在大脑中。然而,其神经生理学效应尚未完全阐明。本研究旨在评估脱落酸对疼痛动物模型的可能镇痛作用,并确定其可能的信号机制。尾闪烁、热板和福尔马林试验用于评估痛觉阈值。所有实验均在雄性 Wistar 大鼠上进行。为了确定过氧化物酶体增殖物激活受体 β/δ(PPARβ/δ)和阿片受体在诱导脱落酸镇痛中的作用,在给予脱落酸前 15 分钟注射了特异性拮抗剂。数据显示,脱落酸(5、10 和 15µg/大鼠,icv)显著降低福尔马林试验中的疼痛反应。此外,它还可以在尾闪烁和热板试验中产生剂量依赖性的镇痛作用。给予 PPARβ/δ拮抗剂(GSK0660,80nM,icv)显著减弱了所有试验中脱落酸的镇痛作用。在尾闪烁和热板试验过程中,纳洛酮(6µg,icv)完全抑制了脱落酸的镇痛作用。结果表明,中枢注射脱落酸具有较强的镇痛作用,部分通过 PPARβ/δ 和阿片信号传导介导。