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本研究旨在探讨前列腺素在炎性痛维持中的作用。大鼠右侧足跖皮下注射角叉菜胶1 h后,于炎症局部注射环氧合酶非选择性抑制剂吲哚美锌,测定大鼠对伤害性热刺激的缩足反射潜伏期(paw withdrawal latency,PWL)。用免疫组织化学、ELISA和RT-PCR方法检测炎症组织中β-内啡肽(β-END)和μ-阿片受体(μopioid receptor,MOR)的表达。结果显示,吲哚美锌能够剂量依赖性地延长大鼠在第2天和第3天的PWL,显著超过正常基础值,产生痛觉减退;吲哚美锌痛觉减退作用可被阿片受体非选择性抑制剂纳洛酮所翻转;吲哚美锌可显著提高模型大鼠炎症组织内β-END阳性细胞数量、β-END蛋白含量及MOR m RNA表达水平。本研究揭示了前列腺素致痛的新机制,即抑制炎症引起的内源性阿片活动,为开发以抑制外周炎症组织前列腺素为目标的镇痛药提供了新的理论依据。
This study aimed to investigate the role of prostaglandins in the maintenance of inflammatory pain. Rats were injected subcutaneously with carrageenan for 1 h on the right foot of the rat. Local indomethazine, a non-selective inhibitor of cyclooxygenase, was injected intraperitoneally into the rats. The paw withdrawal latency latency, PWL). The expression of β-END and μ-opioid receptor (MOR) in inflammatory tissues were detected by immunohistochemistry, ELISA and RT-PCR. The results showed that zinc indomethacin dose-dependently prolonged PWL in rats on day 2 and day 3, significantly higher than the normal basal value, resulting in pain relief; indomethacin loss of pain can be opioid receptor non-selection Naloxone reversed the expression of indomethacin, and the number of β-END positive cells, β-END protein content and MOR m RNA expression in inflammatory tissues of model rats were significantly increased. This study revealed a new mechanism of prostaglandin pain, that is, inhibition of endogenous opioid inflammation caused by inflammation, providing a new theoretical basis for the development of analgesics targeting inhibition of peripheral inflammatory tissue prostaglandins.