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<p>This study aimed to investigate the antitumor effects and underlying mechanisms of β-boswellic acid (β-BA) in glioblastoma (GBM). U251 and U87 cells were treated with β-BA, and cell growth, migration/invasion, pyroptosis, and mitochondrial function were evaluated using viability, proliferation, LDH release, immunofluorescence, ultrastructure, and Western blot assays. In vivo efficacy was assessed in a U251 xenograft mouse model. β-BA significantly inhibited GBM cell proliferation, migration, and invasion in a dose-dependent manner. β-BA induced mitochondrial structural disruption, loss of mitochondrial membrane potential, and excessive ROS accumulation, which activated the NLRP3 inflammasome and triggered pyroptosis, as evidenced by elevated cleaved Caspase-1, GSDMD-N, and ASC expression. MCC950 partially reversed these effects, confirming NLRP3 involvement. In vivo, β-BA markedly reduced tumor growth and consistently induced mitochondrial damage, NLRP3 activation, pyroptosis execution, decreased Ki-67/PCNA levels, and suppression of EMT progression. β-BA exerts potent anti-GBM activity by inducing mitochondrial dysfunction and NLRP3-mediated pyroptosis, providing a mechanistic basis for developing β-BA as a promising natural therapeutic candidate for GBM.</p>

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Mitochondria-mediated pyroptosis: anti-glioblastoma mechanism of the frankincense-derived compound β-boswellic acid

  • 期刊论文

  • 发表日期：

    2026年1月14日

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  • Ning Tang,
  • Hao Wang,
  • Menghao He,
  • Nuojin Geng,
  • Xueling Zhao,
  • Xinhua Zhu,
  • Renyi Yang,
  • Jun Gao,
  • Chunhua Hang

摘要

This study aimed to investigate the antitumor effects and underlying mechanisms of β-boswellic acid (β-BA) in glioblastoma (GBM). U251 and U87 cells were treated with β-BA, and cell growth, migration/invasion, pyroptosis, and mitochondrial function were evaluated using viability, proliferation, LDH release, immunofluorescence, ultrastructure, and Western blot assays. In vivo efficacy was assessed in a U251 xenograft mouse model. β-BA significantly inhibited GBM cell proliferation, migration, and invasion in a dose-dependent manner. β-BA induced mitochondrial structural disruption, loss of mitochondrial membrane potential, and excessive ROS accumulation, which activated the NLRP3 inflammasome and triggered pyroptosis, as evidenced by elevated cleaved Caspase-1, GSDMD-N, and ASC expression. MCC950 partially reversed these effects, confirming NLRP3 involvement. In vivo, β-BA markedly reduced tumor growth and consistently induced mitochondrial damage, NLRP3 activation, pyroptosis execution, decreased Ki-67/PCNA levels, and suppression of EMT progression. β-BA exerts potent anti-GBM activity by inducing mitochondrial dysfunction and NLRP3-mediated pyroptosis, providing a mechanistic basis for developing β-BA as a promising natural therapeutic candidate for GBM.