Mollashahi Mahtab, Abbasnejad Mehdi, Esmaeili-Mahani Saeed
Shahid Bahonar University of Kerman, Faculty of Sciences, Department of Biology, Kerman, Iran.
Kerman University of Medical Sciences, Kerman Neuroscience Research Center (KNRC), Laboratory of Molecular Neuroscience, Kerman, Iran.
Arq Neuropsiquiatr. 2020 Jan;78(1):21-27. doi: 10.1590/0004-282X20190137.
The phytohormone abscisic acid (ABA) as a signaling molecule exists in various types of organisms from early multicellular to animal cells and tissues. It has been demonstrated that ABA has an antinociceptive effect in rodents. The present study was designed to assess the possible role of PKA and phosphorylated ERK (p-ERK) on the antinociceptive effects of intrathecal (i.t.) ABA in male Wistar rats.
The animals were cannulated intrathecally and divided into different experimental groups (n=6‒7): Control (no surgery), vehicle (received ABA vehicle), ABA-treated groups (received ABA in doses of 10 or 20 µg/rat), ABA plus H.89 (PKA inhibitor)-treated group which received the inhibitor 15 min prior to the ABA injection. Tail-flick and hot-plate tests were used as acute nociceptive stimulators to assess ABA analgesic effects. p-ERK was evaluated in the dorsal portion of the spinal cord using immunoblotting.
Data showed that a microinjection of ABA (10 and 20 µg/rat, i.t.) significantly increased the nociceptive threshold in tail flick and hot plate tests. The application of PKA inhibitor (H.89, 100 nM/rat) significantly inhibited ABA-induced analgesic effects. Expression of p-ERK was significantly decreased in ABA-injected animals, which were not observed in the ABA+H.89-treated group.
Overall, i.t. administration of ABA (10 µg/rat) induced analgesia and p-ERK down-expression likely by involving the PKA-dependent mechanism.
植物激素脱落酸(ABA)作为一种信号分子存在于从早期多细胞生物到动物细胞和组织的各类生物体中。已证明ABA在啮齿动物中具有抗伤害感受作用。本研究旨在评估蛋白激酶A(PKA)和磷酸化细胞外信号调节激酶(p-ERK)在雄性Wistar大鼠鞘内注射(i.t.)ABA的抗伤害感受作用中可能发挥的作用。
对动物进行鞘内置管,并分为不同实验组(n = 6 - 7):对照组(未手术)、溶剂组(接受ABA溶剂)、ABA处理组(接受10或20 μg/大鼠剂量的ABA)、ABA加H.89(PKA抑制剂)处理组,该组在注射ABA前15分钟接受抑制剂。甩尾试验和热板试验用作急性伤害性刺激以评估ABA的镇痛作用。使用免疫印迹法在脊髓背侧评估p-ERK。
数据显示,鞘内注射ABA(10和20 μg/大鼠)在甩尾试验和热板试验中显著提高了伤害感受阈值。应用PKA抑制剂(H.89,100 nM/大鼠)显著抑制了ABA诱导的镇痛作用。在注射ABA的动物中p-ERK表达显著降低,而在ABA + H.89处理组中未观察到这种情况。
总体而言,鞘内注射ABA(10 μg/大鼠)可能通过涉及PKA依赖性机制诱导镇痛和p-ERK表达下调。