Selective Cytotoxic and Redox-Associated Effects of Plant-Derived Terpenoids in Human Glioblastoma Cells
Cell Biochemistry and Biophysics, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s12013-026-02122-z
- Dergi Adı: Cell Biochemistry and Biophysics
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Anahtar Kelimeler: Glioblastoma, Terpenoids, Selectivity index, Caspase-3, TAS/TOS
- Atatürk Üniversitesi Adresli: Evet
Özet
Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor and remains highly resistant to standard therapies. Because redox homeostasis is frequently altered in GBM, small natural products that affect viability together with oxidative-stress endpoints may provide promising leads for further development. Here, we evaluated the terpenoids α-pinene, farnesene, carvone, and terpinolene for cytotoxicity and selectivity in human glioblastoma (U87MG) cells compared with primary human dermal fibroblasts (HDFa). Cell viability was assessed by the MTT assay, and nuclear morphology was evaluated using Hoechst 33,258 staining. Apoptosis-related effects were examined by measuring caspase-3 activity, and oxidative balance was assessed using total antioxidant status (TAS) and total oxidant status (TOS) assays. The terpenoids reduced U87MG viability in a concentration-dependent manner while showing substantially lower toxicity in HDFa cells. At 30 µg/mL, all tested terpenoids increased caspase-3 activity in U87MG cells and were associated with increased TAS and decreased TOS relative to control. Overall, these findings identify these terpenoids as selective in vitro hits against U87MG cells and support follow-up studies incorporating direct ROS profiling and expanded apoptosis assays to clarify mechanism.