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Journals / Adıyaman Üniversitesi Sağlık Bilimleri Dergisi / 2026 / Cilt: 12 Sayı: 2

Redox balance, inflammatory signaling, and apoptotic responses to melatonin and caffeic acid phenethyl ester in glioma cells

Glioma hücrelerinde melatonin ve kafeik asit fenetil esterin redoks dengesi, inflamatuvar sinyalleme ve apoptotik yanıtlar üzerine etkileri

Mehmet Emre Yıldırım(SAĞLIK BİLİMLERİ ÜNİVERSİTESİ, ANKARA SAĞLIK UYGULAMA VE ARAŞTIRMA MERKEZİ)0000-0001-7039-2706
Berkay Ayhan(SAĞLIK BİLİMLERİ ÜNİVERSİTESİ, ANKARA SAĞLIK UYGULAMA VE ARAŞTIRMA MERKEZİ)0000-0001-9746-1492
Pages
126–137
Publication Date
2026-08-20
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Melatonin–CAPE combination exerts synergistic cytotoxic and anti-inflammatory effects in glioma cells.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: To evaluate the individual and combined effects of melatonin and caffeic acid phenethyl ester on glioma cell viability, oxidative stress, inflammation, and apoptosis.
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Key Findings & Data:Materials and Methods: U87-MG cells were treated with melatonin (100–200 µM) and CAPE (10–20 µM), alone or combined, for 24 h.
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Conclusion & Impact:Conclusion: Melatonin–CAPE combination exerts synergistic cytotoxic and anti-inflammatory effects in glioma cells.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:Melatonin · Kafeik asit fenetil ester · Glioma

Abstract

Aim: To evaluate the individual and combined effects of melatonin and caffeic acid phenethyl ester on glioma cell viability, oxidative stress, inflammation, and apoptosis. Materials and Methods: U87-MG cells were treated with melatonin (100–200 µM) and CAPE (10–20 µM), alone or combined, for 24 h. Viability (MTT), oxidative stress (ROS, TOS, TAC, OSI), mitochondrial function (JC-1), apoptosis (Annexin V/PI, caspase-3/7), and cytokines (IL-6, TNF-α) were assessed. Drug interactions were analyzed using Bliss independence and combination index (CI). Results: Combined treatment reduced viability to 52% and exceeded Bliss predictions (CI = 0.72), indicating synergy. Oxidative stress decreased, antioxidant capacity increased, mitochondrial depolarization and apoptosis increased, and cytokines were suppressed. Conclusion: Melatonin–CAPE combination exerts synergistic cytotoxic and anti-inflammatory effects in glioma cells.

Özet

Amaç: Melatonin ve CAPE’nin glioma hücrelerinde hücre canlılığı, oksidatif stres, inflamasyon ve apoptoz üzerindeki etkileri incelendi. Gereç ve Yöntem: U87-MG hücreleri melatonin (100–200 µM) ve CAPE (10–20 µM) ile 24 saat tedavi edildi. Hücre canlılığı, oksidatif stres, mitokondriyal fonksiyon, apoptoz ve sitokin düzeyleri değerlendirildi. Bulgular: Kombinasyon tedavisi hücre canlılığını %52’ye düşürdü ve sinerjik etki gösterdi (CI=0,72). Oksidatif stres azaldı, apoptoz arttı. Sonuç: Melatonin–CAPE kombinasyonu sinerjik etki göstermektedir.

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Cite This Article

Yıldırım, M. E., Ayhan, B. (2026). Redox balance, inflammatory signaling, and apoptotic responses to melatonin and caffeic acid phenethyl ester in glioma cells. Adıyaman Üniversitesi Sağlık Bilimleri Dergisi, Cilt: 12 Sayı: 2, 126–137. https://doi.org/10.30569/adiyamansaglik.1867632

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References (16)

  1. Omuro A, DeAngelis LM. Glioblastoma and other malignant gliomas: a clinical review. JAMA. 2013;310(17):1842-1850.
  2. Liu S, Wang J, Yang H, Zhang X, Liu Y. Targeting oxidative stress as a promising strategy to treat glioma. Oxid Med Cell Longev. 2022;2022:921070.
  3. Dinarello CA. Proinflammatory cytokines. Chest. 2000;118(2):503-508.
  4. Reiter RJ, Mayo JC, Tan DX, Sainz RM, Alatorre-Jimenez M, Qin L. Melatonin as an antioxidant: under promises but over delivers. J Pineal Res. 2016;61(3):253-278.
  5. Moretti E, Favero G, Rodella LF, Rezzani R. Melatonin’s antineoplastic potential against glioblastoma: a review. Anticancer Agents Med Chem. 2020;20(3):367-374.
  6. Natarajan K, Singh S, Burke TR, Grunberger D, Aggarwal BB. Caffeic acid phenethyl ester is a potent and specific inhibitor of activation of nuclear transcription factor NF-κB. Proc Natl Acad Sci U S A. 1996;93(17):9090-9095.
  7. Kuo HC, Lin YT, Chou FP, Wang CC, Hung HC, Chen YW. Inhibitory effect of caffeic acid phenethyl ester on the growth of C6 glioma cells in vitro and in vivo. Cancer Lett. 2006;234(2):199-208.
  8. Armutcu F, Akyol S, Ustunsoy S, Turan FF. Therapeutic potential of caffeic acid phenethyl ester and its anti-inflammatory and immunomodulatory effects. Exp Ther Med. 2015;9(5):1582-1588.
  9. Murtaza G, Sajjad A, Mehmood Z, Shah SH, Siddiqi AR. Possible molecular targets for therapeutic applications of caffeic acid phenethyl ester in inflammation and cancer. J Food Drug Anal. 2015;23(1):11-18.
  10. Mosmann T. Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. J Immunol Methods. 1983;65(1-2):55-63.
  11. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38(12):1103-1111.
  12. LeBel CP, Ischiropoulos H, Bondy SC. Evaluation of the probe 2′,7′-dichlorofluorescin as an indicator of reactive oxygen species formation and oxidative stress. Chem Res Toxicol. 1992;5(2):227-231.
  13. Vermes I, Haanen C, Steffens-Nakken H, Reutelingsperger C. A novel assay for apoptosis: flow cytometric detection of phosphatidylserine expression on early apoptotic cells using fluorescein-labelled Annexin V. J Immunol Methods. 1995;184(1):39-51.
  14. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔCT method. Methods. 2001;25(4):402-408.
  15. Wang J, Hao H, Yao L, Zhang X, Zhao S, Ling EA. Melatonin suppresses migration and invasion via inhibition of oxidative stress pathway in glioma cells. J Pineal Res. 2012;53(2):180-187.
  16. Moretti E, Favero G, Rodella LF, Rezzani R. Melatonin's antineoplastic potential against glioblastoma: a review. Cells. 2020;9(3):599.