Abstract：
Bone cancer pain (BCP) profoundly impacts patient\'s quality of life, demanding more effective pain management strategies. The aim of this systematic review was to investigate the role of inflammatory cytokines as potential molecular targets in BCP. A systematic search for animal rodent models of bone cancer pain studies was conducted in PubMed, Scopus, and Web of Science. Methodological quality and risk of bias were assessed using the SYRCLE RoB tool. Twenty-five articles met the inclusion criteria, comprising animal studies investigating molecular targets related to inflammatory cytokines in BCP. A low to moderate risk of bias was reported. Key findings in 23 manuscripts revealed upregulated classic pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-17, IL-18, IL-33) and chemokines in the spinal cord, periaqueductal gray, and dorsal root ganglia. Interventions targeting these cytokines consistently mitigated pain behaviors. Additionally, it was demonstrated that glial cells, due to their involvement in the release of inflammatory cytokines, emerged as significant contributors to BCP. This systematic review underscores the significance of inflammatory cytokines as potential molecular targets for alleviating BCP. It emphasizes the promise of targeted interventions and advocates for further research to translate these findings into effective therapeutic strategies. Ultimately, this approach holds the potential to enhance the patient\'s quality of life.
摘要：
骨癌疼痛（BCP）深刻影响患者的生活质量，需要更有效的疼痛管理策略。本系统综述的目的是研究炎性细胞因子作为BCP潜在分子靶标的作用。在PubMed中对骨癌疼痛研究的动物啮齿动物模型进行了系统的搜索，Scopus,和WebofScience。使用SYRCLERoB工具评估方法学质量和偏倚风险。25条符合纳入标准,包括研究与BCP中炎症细胞因子相关的分子靶标的动物研究。报告了低至中度的偏倚风险。在23份手稿中的关键发现揭示了上调的经典促炎细胞因子（TNF-α，IL-1β,IL-6，IL-17，IL-18，IL-33）和趋化因子在脊髓，导水管周围灰色,和背根神经节.针对这些细胞因子的干预一致地减轻疼痛行为。此外,已经证明神经胶质细胞，由于它们参与炎症细胞因子的释放，成为BCP的重要贡献者。本系统综述强调了炎性细胞因子作为缓解BCP的潜在分子靶标的重要性。它强调有针对性的干预措施的承诺，并倡导进一步研究，以将这些发现转化为有效的治疗策略。最终,这种方法有可能提高患者的生活质量。
