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褪黑素通过抑制NF-κB/COX-2信号通路增强替莫唑胺对胶质母细胞瘤的化疗效果。

Melatonin Synergises the Chemotherapeutic Effect of Temozolomide in Glioblastoma by Suppressing NF-κB/COX-2 Signalling Pathways.

作者信息

Tang Hong, Dai Qi, Zhao Ziyan, Ge Weiye, Li Danlei, Chang Zelin, Pi Penglai, Li Jia, Sun Zheng

机构信息

Department of Integrated Medicine, College of Integrated Medicine, Dalian Medical University, Dalian, People's Republic of China.

The First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China.

出版信息

J Cell Mol Med. 2025 Aug;29(15):e70778. doi: 10.1111/jcmm.70778.

DOI:10.1111/jcmm.70778
PMID:40804775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12350191/
Abstract

Glioblastoma (GBM) is an aggressive and highly malignant primary brain tumour, accounting for a significant proportion of adult brain tumours. It is associated with a poor prognosis and high recurrence rates. Although temozolomide (TMZ) remains the standard first-line chemotherapy for GBM, its clinical efficacy is often limited by the development of drug resistance and toxic effects on normal tissues. Melatonin (Mel), a natural indoleamine synthesised by the pineal gland, has demonstrated synergistic anti-tumour effects when combined with various chemotherapy agents in multiple studies. This study investigates the synergistic potential of Mel to enhance TMZ's therapeutic efficacy against GBM. The results demonstrate that the combination of Mel and TMZ significantly inhibits glioblastoma cell proliferation, migration, and invasion. Mechanistically, this synergistic effect is mediated through the NF-κB/COX-2 signalling pathway. Mel enhances TMZ's anti-tumour activity by inhibiting IκBα phosphorylation, suppressing NF-κB activation, and downregulating COX-2 expression. Additionally, the combination treatment induced apoptosis via activation of the Caspase-3 pathway. These results suggest that Mel can potentiate the therapeutic efficacy of TMZ in glioblastoma treatment, offering a promising strategy to overcome TMZ resistance while reducing its associated toxicity.

摘要

胶质母细胞瘤(GBM)是一种侵袭性强、高度恶性的原发性脑肿瘤,在成脑肿瘤中占相当大的比例。它与预后不良和高复发率相关。尽管替莫唑胺(TMZ)仍然是GBM的标准一线化疗药物,但其临床疗效常常受到耐药性的发展以及对正常组织的毒性作用的限制。褪黑素(Mel)是一种由松果体合成的天然吲哚胺,在多项研究中,它与各种化疗药物联合使用时已显示出协同抗肿瘤作用。本研究调查了Mel增强TMZ对GBM治疗效果的协同潜力。结果表明,Mel与TMZ联合使用可显著抑制胶质母细胞瘤细胞的增殖、迁移和侵袭。从机制上讲,这种协同效应是通过NF-κB/COX-2信号通路介导的。Mel通过抑制IκBα磷酸化、抑制NF-κB激活和下调COX-2表达来增强TMZ的抗肿瘤活性。此外,联合治疗通过激活Caspase-3途径诱导细胞凋亡。这些结果表明,Mel可以增强TMZ在胶质母细胞瘤治疗中的疗效,为克服TMZ耐药性同时降低其相关毒性提供了一种有前景的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/2da6f0b61d46/JCMM-29-e70778-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/6a194f0ce2e3/JCMM-29-e70778-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/e89489b1933a/JCMM-29-e70778-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/fe19d20a6e3b/JCMM-29-e70778-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/72cfdaf8f960/JCMM-29-e70778-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/47eacdacbfae/JCMM-29-e70778-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/5f7558b69459/JCMM-29-e70778-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/13915de3b77e/JCMM-29-e70778-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/fadf2c79979c/JCMM-29-e70778-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/2da6f0b61d46/JCMM-29-e70778-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/6a194f0ce2e3/JCMM-29-e70778-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/e89489b1933a/JCMM-29-e70778-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/fe19d20a6e3b/JCMM-29-e70778-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/72cfdaf8f960/JCMM-29-e70778-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/47eacdacbfae/JCMM-29-e70778-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/5f7558b69459/JCMM-29-e70778-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/13915de3b77e/JCMM-29-e70778-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/fadf2c79979c/JCMM-29-e70778-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5856/12350191/2da6f0b61d46/JCMM-29-e70778-g006.jpg

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本文引用的文献

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Melatonin, an Antitumor Necrosis Factor Therapy.褪黑素,一种抗肿瘤坏死因子疗法。
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The effect of Licochalcone A on proliferation, invasion, and drug resistance of glioma cells by regulating TLR4/NF-κB signaling pathway.
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