Área Académica de Medicina del Instituto de Ciencias de la Salud. Universidad Autónoma del Estado de Hidalgo, Pachuca, Hidalgo, Mexico.
Área Académica de Gerontología del Instituto de Ciencias de la Salud. Universidad Autónoma del Estado de Hidalgo, Pachuca, Hidalgo, Mexico.
Can J Physiol Pharmacol. 2021 Oct;99(10):1048-1056. doi: 10.1139/cjpp-2020-0744. Epub 2021 Apr 15.
The aim of this study was to examine if the peripheral antinociception of α-bisabolol involves the participation of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) synthesis followed by K channel opening in the formalin test. Wistar rats were injected in the dorsal surface of the right hind paw with formalin (1%). Rats received a subcutaneous injection into the dorsal surface of the paw of vehicles or increasing doses of α-bisabolol (100-300 µg/paw). To determine whether the peripheral antinociception induced by α-bisabolol was mediated by either the opioid receptors or the NO-cGMP-K channels pathway, the effect of pretreatment (10 min before formalin injection) with the appropriate vehicles, naloxone, naltrexone, N-nitro-l-arginine methyl ester (L-NAME), 1H-[1,2,4]-oxadiazolo[4,2-a]quinoxalin-1-one (ODQ), glibenclamide, glipizide, apamin, charybdotoxin, tetraethylammonium, or 4-aminopyridine on the antinociceptive effects induced by local peripheral α-bisabolol (300 µg/paw) were assessed. α-Bisabolol produced antinociception during both phases of the formalin test. α-Bisabolol antinociception was blocked by L-NAME, ODQ, and all the K channels blockers. The peripheral antinociceptive effect produced by α-bisabolol was not blocked by the opioid receptor inhibitors. α-Bisabolol was able to active the NO-cGMP-K channels pathway to produce its antinoceptive effect. The participation of opioid receptors in the peripheral local antinociception induced by α-bisabolol is excluded.
本研究旨在考察 α- 姜黄醇的外周抗伤害作用是否涉及一氧化氮 (NO) 和环鸟苷酸 (cGMP) 合成的参与，随后在福尔马林试验中打开 K 通道。Wistar 大鼠右后爪背部表面注射福尔马林（1%）。大鼠在爪背部表面接受皮下注射载体或递增剂量的 α- 姜黄醇（100-300μg/爪）。为了确定 α- 姜黄醇诱导的外周镇痛是否通过阿片受体或 NO-cGMP-K 通道途径介导，用适当的载体、纳洛酮、纳曲酮、N- 硝基-L-精氨酸甲酯 (L-NAME)、1H-[1,2,4]-恶二唑[4,2-a]喹喔啉-1-酮 (ODQ)、格列本脲、格列吡嗪、阿帕米胺、沙蟾毒素、四乙铵或 4- 氨基吡啶预处理（在福尔马林注射前 10 分钟），评估其对局部外周 α- 姜黄醇（300μg/爪）诱导的镇痛作用的影响。α- 姜黄醇在福尔马林试验的两个阶段均产生镇痛作用。α- 姜黄醇的镇痛作用被 L-NAME、ODQ 和所有 K 通道阻滞剂阻断。阿片受体抑制剂不能阻断 α- 姜黄醇产生的外周镇痛作用。α- 姜黄醇能够激活 NO-cGMP-K 通道途径产生其镇痛作用。排除了阿片受体参与 α- 姜黄醇诱导的外周局部镇痛作用。
