Chronic inflammation is a well-established hallmark of cancer, playing a critical role in the initiation and progression of gliomas. Recent evidence underscores the importance of anti-inflammatory natural products as chemotherapeutic and potentially as chemopreventive agents, offering a safe and multifaceted approach to mitigate tumor-promoting inflammation in the brain. This review explores the interplay between major inflammation-related pathways—such as NF-κB, COX-2, and the NLRP3 inflammasome—and key bioactive compounds derived from natural sources such as polyphenols, isothiocyanates, terpenes/lignans, and omega-3-derived mediators. We provide evidence on the effect of these compounds on the above inflammatory triangle. We discuss emerging in vitro, in vivo preclinical and translational evidence in the context of glioma biology and highlight how these compounds may pass the blood–brain barrier (BBB) and modulate the tumor microenvironment (TME), including immune cell infiltration and cytokine profiles that may act in a pro- or anti-inflammatory manner, highlighting their capacity to inhibit GBM-associated inflammation. Each substance may differentially influence the components of the inflammatory triangle. Overall, we position these agents as low-toxicity, formulation-aware adjuncts to standard care. The ultimate goal is offering novel insights on low-toxicity, inflammation-targeting interventions against malignant brain tumors.
慢性炎症是癌症的公认标志之一,在胶质瘤的发生发展中起着关键作用。最新研究证据强调了抗炎天然产物作为化疗药物及潜在化学预防剂的重要性,为抑制脑内促瘤性炎症提供了安全且多靶点的干预策略。本综述探讨了NF-κB、COX-2及NLRP3炎症小体等主要炎症相关通路与多酚类、异硫氰酸盐、萜类/木脂素及ω-3衍生介质等天然来源生物活性化合物之间的相互作用。我们系统论证了这些化合物对上述"炎症三角"调控网络的干预效应,结合胶质瘤生物学特性,重点讨论了体外实验、临床前动物模型及转化医学研究的最新进展,阐释了这些化合物穿透血脑屏障、调节肿瘤微环境(包括免疫细胞浸润及促炎/抗炎细胞因子谱)的作用机制,揭示其抑制胶质母细胞瘤相关炎症的潜力。不同化合物可能对炎症三角的组分产生差异化调控。总体而言,我们认为这些天然产物可作为低毒性、剂型优化的辅助治疗手段,与标准疗法协同应用。本文旨在为针对恶性脑肿瘤的低毒性炎症靶向治疗策略提供新的理论视角。