Comparison of prostaglandin E1- and prostaglandin E2-induced hyperalgesia in the rat
Comparison of prostaglandin E1- and prostaglandin E2-induced hyperalgesia in the rat
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DOI：
10.1016/0306-4522(94)90369-7
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发表时间：
1994-09
期刊：
影响因子：
3.3
通讯作者：
S. Khasar;T. Ho;P. Green;Jon D. Levine
中科院分区：
文献类型：
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作者：
S. Khasar;T. Ho;P. Green;Jon D. Levine
我们通过在正常和链脲佐菌素诱导的糖尿病大鼠中单独注射前列腺素E1或与其他药物一起注射之前和之后评估缩足阈值，研究了前列腺素E1诱导的大鼠后爪机械性痛觉过敏。在正常和糖尿病大鼠中，前列腺素E1（1-1000 ng）产生剂量依赖性的机械伤害性阈值降低。在糖尿病大鼠中，前列腺素E1比正常大鼠更有效地产生痛觉过敏，而前列腺素E2在正常和糖尿病大鼠中的痛觉过敏没有改变。在正常或糖尿病大鼠中，前列腺素Ei诱导的痛觉过敏不被E型1前列腺素受体拮抗剂SC 19220或SC 51089抑制。事实上，在SC 19220的存在下，前列腺素E1在正常大鼠中产生增强的痛觉过敏。前列腺素E1痛觉过敏没有显着修改交感神经切除术或吲哚美辛。与前列腺素E2不同的是，前列腺素E1的痛觉过敏不能被刺激性鸟嘌呤核苷酸结合调节蛋白鸟苷5 '-O-抑制剂阻断。（2-硫代二磷酸）。这表明前列腺素E1通过激活除E1型前列腺素受体以外的前列腺素受体，并且该受体不与刺激性鸟嘌呤核苷酸结合调节蛋白偶联。
We have studied prostaglandin E1-induced mechanical hyperalgesia in the rat hindpaw, by assessing paw-withdrawal thresholds, before and after injecting prostaglandin E1alone or with other agents, in normal and streptozotocin-induced diabetic rats. In normal and diabetic rats, prostaglandin E1(1–1000 ng) produced a dose-dependent decrease in mechanical nociceptive threshold. In diabetic rats, prostaglandin E1was more potent than in normal rats, in producing hyperalgesia, whereas prostaglandin E2hyperalgesia was not changed in normal and diabetic rats. Prostaglandin Ei-induced hyperalgesia was not inhibited by E-type 1 prostaglandin receptor antagonists, SC 19220 or SC51089, either in normal or diabetic rats. In fact, in the presence of SC19220, prostaglandin E1produced enhanced hyperalgesia, in normal rats. Prostaglandin E1hyperalgesia was not significantly modified by sympathectomy or indomethacin. Unlike prostaglandin E2, prostaglandin E1hyperalgesia was not blocked by the inhibitor of the stimulatory guanine nucleotide-binding regulatory protein, guanosine 5'-O-(2-thiodiphosphate).It is suggested that prostaglandin E1decreases primary afferent nociceptive threshold directly, by activating a prostaglandin receptor other than the E-type 1 prostaglandin receptor, and that this receptor is not coupled to a stimulatory guanine nucleotide-binding regulatory protein.