Marotti T, Balog T, Mazuran R, Rocić B
Department of Biology and Medicine, Ruder Bosković Institute, Zagreb, Croatia.
Neuropeptides. 1998 Feb;32(1):57-62. doi: 10.1016/s0143-4179(98)90017-8.
In the present study the in vitro and in vivo effect of Met-enkephalin (MENK) on nitric oxide (NO) release by mouse peritoneal macrophages was evaluated. While in vitro MENK was ineffective unless combined with suboptimal concentrations of recombinant murine interferon gamma, in vivo all the doses (2.5, 5 or 10 mg/kg bw) bimodaly modulated NO release. Only the stimulative (2.5 and 10 mg/kg bw) and not the suppressive (5 mg/kg bw) dose of MENK was opioid receptor-mediated as demonstrated by abolishing the effect by naloxone. The stimulative effect of the low (2.5 mg/kg bw) dose, that was observed only if MENK was injected p.m., was associated with the IL production and IFN gamma as demonstrated by abolishing the effect by specific antibodies. The data additionally support the idea that opioid-mediated responses might be to a large degree mediated by the release of cytokines.
在本研究中，评估了甲硫氨酸脑啡肽（MENK）对小鼠腹腔巨噬细胞释放一氧化氮（NO）的体外和体内效应。体外实验中，除非与次优浓度的重组鼠干扰素γ联合使用，否则MENK无效；而在体内实验中，所有剂量（2.5、5或10mg/kg体重）均对NO释放产生双峰调节作用。只有MENK的刺激剂量（2.5和10mg/kg体重）而非抑制剂量（5mg/kg体重）是由阿片受体介导的，这通过纳洛酮消除其作用得到证实。低剂量（2.5mg/kg体重）的刺激作用仅在下午注射MENK时观察到，且与白细胞介素产生和干扰素γ有关，这通过特异性抗体消除其作用得到证实。这些数据进一步支持了阿片介导的反应可能在很大程度上由细胞因子释放介导的观点。
