小胶质细胞
神经炎症
炎症
神经保护
吗啡
癌症疼痛
癌症
神经毒性
免疫系统
免疫学
生物
医学
药理学
神经科学
内科学
毒性
作者
Houan Tu,Haichen Chu,Sen Guan,Fengxi Hao,Na Xu,Zhiping Zhao,Yongxin Liang
出处
期刊:Tissue & Cell
[Elsevier]
日期:2021-02-01
卷期号:68: 101438-101438
被引量:30
标识
DOI:10.1016/j.tice.2020.101438
摘要
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.
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