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<p>Pyroptosis is a pro-inflammatory programmed cell death linked to inflammation. While animal venoms can trigger pyroptosis, it remains unknown whether the venom of the neurotoxic snake <i>Bungarus multicinctus</i> (BM) can induce pyroptosis in microglia. This study aimed to investigate this process in mouse BV2 microglia. We exposed cells to BM venom and assessed viability, pyroptosis markers, and inflammation. To further verify this, we added the pyroptosis inhibitor disulfiram (5&#xa0;μmol/L) to the experimental system. Subsequent assays revealed that exposure to BM venom led to a dose‑dependent suppression of cellular viability. Concurrently, this venom treatment upregulated the levels of pyroptosis‑associated proteins, namely NLRP3, GSDMD‑N, and Caspase‑1 p20. Moreover, it elevated the mRNA transcripts of IL‑1β, TNF‑α, and IL‑6, while also stimulating the secretion of both IL‑1β and IL‑18. The venom also enhanced propidium iodide uptake, indicating membrane damage. These pyroptotic and inflammatory effects were attenuated by antivenom and the pyroptosis inhibitor disulfiram. In conclusion, BM venom induces pyroptosis and neuroinflammation in microglia.</p>

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Bungarus multicinctus venom induces pyroptosis via the NLRP3/Caspase-1/GSDMD pathway in BV2 cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月30日

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  • Mei Luo,
  • Zeng-Rui Wang,
  • Xing-Ling Tan,
  • Xia Yang,
  • Zong Ning

摘要

Pyroptosis is a pro-inflammatory programmed cell death linked to inflammation. While animal venoms can trigger pyroptosis, it remains unknown whether the venom of the neurotoxic snake Bungarus multicinctus (BM) can induce pyroptosis in microglia. This study aimed to investigate this process in mouse BV2 microglia. We exposed cells to BM venom and assessed viability, pyroptosis markers, and inflammation. To further verify this, we added the pyroptosis inhibitor disulfiram (5 μmol/L) to the experimental system. Subsequent assays revealed that exposure to BM venom led to a dose‑dependent suppression of cellular viability. Concurrently, this venom treatment upregulated the levels of pyroptosis‑associated proteins, namely NLRP3, GSDMD‑N, and Caspase‑1 p20. Moreover, it elevated the mRNA transcripts of IL‑1β, TNF‑α, and IL‑6, while also stimulating the secretion of both IL‑1β and IL‑18. The venom also enhanced propidium iodide uptake, indicating membrane damage. These pyroptotic and inflammatory effects were attenuated by antivenom and the pyroptosis inhibitor disulfiram. In conclusion, BM venom induces pyroptosis and neuroinflammation in microglia.