School of Pharmacy, Hubei University of Science and Technology, Xianning 437100, China.
Research Center of Basic Medical Sciences, Department of Physiology, School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning 437100, China.
Acta Biochim Biophys Sin (Shanghai). 2020 Mar 18;52(3):231-240. doi: 10.1093/abbs/gmz162.
Bone cancer pain (BCP) is induced by primary bone cancer and secondary bone metastasis. During BCP pathogenesis, activated spinal astrocytes release proinflammatory cytokines, which participate in pain information transmission. In this study, we found that BCP rats showed disruption of trabecular bone structure, mechanical allodynia, and spinal inflammation. Moreover, reduced adenosine monophosphate-activated protein kinase (AMPK) activity, increased mitochondrial fission-associated protein Drp1 GTPase activity accompanied by the dysfunction of mitochondrial function, and abnormal BAX and Bcl-2 expression were found in the spinal cord of BCP rats. Notably, these alterations are reversed by resveratrol (Res) administration. Cell experiment results demonstrated that Res promotes mitochondrial function by activating AMPK, decreasing Drp1 activity, and inhibiting tumor necrosis factor-α-induced mitochondrial membrane potential reduction. Taken together, these results indicate that Res suppresses BCP in rats by attenuation of the inflammatory responses through the AMPK/Drp1 signaling pathway.
骨癌疼痛(BCP)由原发性骨癌和继发性骨转移引起。在 BCP 发病机制中,激活的脊髓星形胶质细胞释放促炎细胞因子,参与疼痛信息传递。在这项研究中,我们发现 BCP 大鼠表现出小梁骨结构破坏、机械性痛觉过敏和脊髓炎症。此外,在 BCP 大鼠的脊髓中还发现,AMPK 活性降低,线粒体分裂相关蛋白 Drp1 GTPase 活性增加伴随着线粒体功能障碍,以及 BAX 和 Bcl-2 表达异常。值得注意的是,这些改变可以通过白藜芦醇(Res)的给药来逆转。细胞实验结果表明,Res 通过激活 AMPK、降低 Drp1 活性和抑制肿瘤坏死因子-α诱导的线粒体膜电位降低来促进线粒体功能。综上所述,这些结果表明,Res 通过 AMPK/Drp1 信号通路抑制炎症反应来抑制大鼠的 BCP。