Effects of Combined Artemisia absinthium and Temozolomide Treatment on Apoptosis, Autophagy, and Nitric Oxide Synthase in Glioblastoma Glioblastomada Artemisia absinthium ve Temozolomidin Kombine Uygulamasının Apoptoz, Otofaji ve Nitrik Oksit Sentaz Üzerine Etkileri


TUĞRUL B., Çöllü F., GÜRCÜ B.

Commagene Journal of Biology, cilt.10, sa.1, ss.80-90, 2026 (Scopus, TRDizin) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 10 Sayı: 1
  • Basım Tarihi: 2026
  • Doi Numarası: 10.31594/commagene.1839245
  • Dergi Adı: Commagene Journal of Biology
  • Derginin Tarandığı İndeksler: Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.80-90
  • Anahtar Kelimeler: cell migration, mitochondrial dysfunction, programmed cell death, T98-G cell line
  • Manisa Celal Bayar Üniversitesi Adresli: Evet

Özet

Artemisia absinthium (wormwood; WO) is a plant known for its anticancer potential and this study comprehensively evaluates the effects of WO, alone and in combination with Temozolomide (TMZ), on cytotoxicity, apoptosis, autophagy, mitochondrial membrane potential, cell migration, and nitric oxide synthase (NOS) responses in T98-G glioblastoma cells. Cytotoxicity, apoptosis, autophagy, mitochondrial membrane potential, and cell migration were assessed using MTT, Annexin V-FITC/PI, JC-1, monodansylcadaverine (MDC) staining, and wound healing assay, respectively. Protein levels of eNOS, iNOS, and LC3-II were examined using immunofluorescence and western blotting. WO significantly reduced T98-G cell viability in a dose- and time-dependent manner with pronounced cytotoxicity observed at 48 and 72 hours. The combined treatment increased early (24.6%) and late (40.5%) apoptosis, reducing cell viability to 31.9%. Combined treatment markedly increased autophagic vacuoles, enhancing perinuclear and cytoplasmic accumulation compared with single agents. Combined WO and TMZ treatment disrupted mitochondrial membrane potential more prominently than either agent alone, suggesting that apoptosis is mediated via the mitochondrial pathway. WO strongly inhibited T98-G cell migration, whereas TMZ and the combination had moderate suppressive effects. In T98-G cells, WO IC50 significantly increased eNOS (p<0.0001), iNOS (p<0.0001), and LC3 (p<0.01), while TMZ IC50 moderately increased iNOS (p<0.05) and combined treatment maximally elevated iNOS and LC3 (p<0.0001) without further affecting eNOS. Preliminary Western blot analyses qualitatively corroborated the immunofluorescence data, indicating consistent treatment-dependent trends in eNOS, iNOS, and LC3-II expression. These findings highlight the potential of WO in enhancing TMZ efficacy and provide a basis for further investigation in glioblastoma therapy.