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首页> 美国卫生研究院文献>other >Antinociceptive Effects of Analgesic-Antitumor Peptide (AGAP) a Neurotoxin from the Scorpion Buthus martensii Karsch on Formalin-Induced Inflammatory Pain through a Mitogen-Activated Protein Kinases–Dependent Mechanism in Mice
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Antinociceptive Effects of Analgesic-Antitumor Peptide (AGAP) a Neurotoxin from the Scorpion Buthus martensii Karsch on Formalin-Induced Inflammatory Pain through a Mitogen-Activated Protein Kinases–Dependent Mechanism in Mice

机译：镇痛抗肿瘤肽（AGAP）一种来自蝎蝎蝎（Bothus martensii Karsch）的神经毒素的抗伤害感受作用通过丝裂素活化的蛋白激酶依赖性小鼠机制对福尔马林诱导的炎性疼痛。

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In the present study, we investigated the anti-nociceptive effect and the underlying mechanism of the analgesic-antitumor peptide (AGAP), a neurotoxin from the scorpion Buthus martensii Karsch. AGAP in doses of 0.2, 1 and 5 µg was injected intraplantarly (i.pl.) before formalin injection 10 min at the same site. The suppression by intraplantar injection of AGAP on formalin-induced spontaneous nociceptive behaviors was investigated. The results show that AGAP could dose-dependently inhibit formalin-induced two-phase spontaneous flinching response. To investigate the mechanism of action of treatment with AGAP in inflammatory pain, the expressions of peripheral and spinal phosphorylated mitogen-activated protein kinases (phospho-MAPKs) including p-p38, p-ERK and p-JNK were examined. We found that formalin increased the expressions of peripheral and spinal MAPKs, which were prevented by pre-intraplantar injection of AGAP in inflammation pain model in mice. AGAP could also decrease the expression of spinal Fos induced by formalin. Furthermore, combinations the lower doses of the inhibitors of MAPKs (U0126, SP600125, or SB203580 0.1 µg) with the lower dose of AGAP (0.2 µg), the results suggested that AGAP could potentiate the effects of the inhibitors of MAPKs on the inflammatory pain. The present results indicate that pre-intraplantar injection of AGAP prevents the inflammatory pain induced by formalin through a MAPKs-mediated mechanism in mice.
机译：在本研究中，我们研究了来自蝎蝎子马氏杆菌Karsch的神经毒素镇痛抗肿瘤肽（AGAP）的抗伤害感受作用及其潜在机制。足底内（i.pl.）足底注射iPAP剂量为0.2、1和5 µg，然后在同一部位注射福尔马林10分钟。研究了足底内注射AGAP对福尔马林诱导的自发伤害行为的抑制作用。结果表明，AGAP可以剂量依赖性地抑制福尔马林诱导的两相自发退缩反应。为了研究AGAP治疗炎性疼痛的作用机制，检查了包括p-p38，p-ERK和p-JNK在内的外周和脊髓磷酸化的丝裂原活化蛋白激酶（phospho-MAPKs）的表达。我们发现福尔马林增加了小鼠炎症痛模型中足底内注射AGAP所阻止的外周和脊髓MAPKs表达。 AGAP还可以降低福尔马林诱导的脊髓Fos的表达。此外，将较低剂量的MAPKs抑制剂（U0126，SP600125或SB203580 0.1 µg）与较低剂量的AGAP（0.2 µg）结合使用，结果表明AGAP可以增强MAPKs抑制剂对炎性疼痛的作用。 。目前的结果表明，足底内注射AGAP可通过MAPKs介导的机制预防福尔马林引起的炎症性疼痛。

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