Cancer pain, especially bone cancer pain, is a pain state often caused by inflammation or dysfunctional nerves. Moreover, in the management of cancer pain, opioid especially morphine is widely used, however, it also brings severe side effects such as morphine tolerance to the patient (Deandrea et al., 2008). A growing body of literatures demonstrated that neuroinflammation is mediated by microglia. As the macrophages like immune cells, microglia play an important role in the pathogenesis of cancer pain and morphine tolerance. Microglia acquire different activation states to regulate the function of these cells. As to M1 phenotype, microglia release pro-inflammatory cytokines and neurotoxic molecules that promote inflammation and cytotoxic reactions. Conversely, when microglia represent M2 phenotypes secreting anti-inflammatory cytokines and nutrient factors that promote the function of repair, regeneration and restore homeostasis. A better understanding of microglia activation in cancer pain and morphine tolerance is crucial for the development of hypothesized neuroprotective drugs. Targeting microglia different polarization states by the inhibition of their deleterious pro-inflammatory neurotoxicity and/or enhancing their beneficial anti-inflammatory protective function seems to be an effective treatment for cancer pain and morphine tolerance.

癌痛，尤其是骨癌痛，是一种常由炎症或神经功能障碍引起的疼痛状态。此外，在癌症疼痛的治疗中，阿片类药物尤其是吗啡被广泛使用，但它也给患者带来了严重的副作用，例如吗啡耐受性（Deandrea et al., 2008）。越来越多的文献表明神经炎症是由小胶质细胞介导的。作为巨噬细胞和免疫细胞一样，小胶质细胞在癌痛和吗啡耐受的发病机制中起着重要作用。小胶质细胞获得不同的激活状态以调节这些细胞的功能。至于 M1 表型，小胶质细胞释放促炎细胞因子和神经毒性分子，促进炎症和细胞毒性反应。反过来，当小胶质细胞代表 M2 表型时，会分泌抗炎细胞因子和营养因子，促进修复、再生和恢复体内平衡的功能。更好地了解癌症疼痛和吗啡耐受中的小胶质细胞激活对于开发假设的神经保护药物至关重要。通过抑制其有害的促炎神经毒性和/或增强其有益的抗炎保护功能来靶向不同极化状态的小胶质细胞似乎是治疗癌痛和吗啡耐受性的有效方法。