Dose-response : a publication of International Hormesis Society · 2026
Total Sanghuangporus vaninii Extract Ameliorates Cisplatin-Induced Glioma Cell Death by Regulating Ferroptosis and Inflammation.
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Xu Yankai, Zhou Jiesi, Zhou Xiaobin, Li Yong, Yang Senyuan, Xue Zebin
Аннотация
OBJECTIVES: Ferroptosis is a distinct form of programmed cell death characterized by iron (Fe)-dependent oxidative stress and the accumulation of intracellular reactive oxygen species. Cisplatin (CPT), a chemotherapeutic agent, can induce ferroptosis in glioma cells and act synergistically with erastin (EST). The total extract of the fungus Sanghuangporus vaninii (TSV) has anticancer and antioxidant activities. This investigation aimed to assess the properties of TSV on CPT-induced inflammatory response and ferroptosis-related changes in glioma cells.
METHODS: LNZ308 glioma cells were exposed to CPT and EST, followed by treatment with different TSV concentrations. Cell viability was assessed. Intracellular reactive oxygen species (ROS), glutathione peroxidase 4 (GPX4), glutathione (GSH), labile iron pool (LIP), LPO, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were examined, and cell migration was assessed using a scratch assay.
RESULTS: TSV (25 µg/mL) exhibited limited toxicity to LNZ308 cells but failed to reverse the CPT-induced loss of cell viability. TSV markedly reduced ROS levels, LIP, and LPO, while restoring GSH and GPX4 levels. Moreover, it diminished IL-1β, TNF-α, and IL-6 in CPT-treated LNZ308 cells in a dose-responsive manner. L-ascorbic acid diminished ROS levels during oxidative stress. TSV also promoted scratch closure in both untreated and CPT-treated LNZ308 cells.
CONCLUSION: The results indicate that TSV modulates CPT-induced oxidative, inflammatory, and ferroptotic responses in LNZ308 glioma cells in vitro, supporting further investigation of its potential as an adjunct to chemotherapy.
METHODS: LNZ308 glioma cells were exposed to CPT and EST, followed by treatment with different TSV concentrations. Cell viability was assessed. Intracellular reactive oxygen species (ROS), glutathione peroxidase 4 (GPX4), glutathione (GSH), labile iron pool (LIP), LPO, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were examined, and cell migration was assessed using a scratch assay.
RESULTS: TSV (25 µg/mL) exhibited limited toxicity to LNZ308 cells but failed to reverse the CPT-induced loss of cell viability. TSV markedly reduced ROS levels, LIP, and LPO, while restoring GSH and GPX4 levels. Moreover, it diminished IL-1β, TNF-α, and IL-6 in CPT-treated LNZ308 cells in a dose-responsive manner. L-ascorbic acid diminished ROS levels during oxidative stress. TSV also promoted scratch closure in both untreated and CPT-treated LNZ308 cells.
CONCLUSION: The results indicate that TSV modulates CPT-induced oxidative, inflammatory, and ferroptotic responses in LNZ308 glioma cells in vitro, supporting further investigation of its potential as an adjunct to chemotherapy.