Bungarus multicinctus venom induces pyroptosis via the NLRP3/Caspase-1/GSDMD pathway in BV2 cells
- 1Department of General Practice, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, 530021 Guangxi China
- 2Department of General Practice, Baise People’s Hospital, No.8 Chengxiang Road, Baise, 533000 Guangxi China
Abstract
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.
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BibTeX
@article{luo2026bungarus,
title = {{Bungarus multicinctus venom induces pyroptosis via the NLRP3/Caspase-1/GSDMD pathway in BV2 cells}},
author = {Mei Luo and Zeng-Rui Wang and Xing-Ling Tan and Xia Yang and Zong Ning},
journal = {Cell Biology and Toxicology},
year = {2026},
month = jul,
doi = {10.1007/s10565-026-10240-w},
url = {https://doi.org/10.1007/s10565-026-10240-w},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Bungarus multicinctus venom induces pyroptosis via the NLRP3/Caspase-1/GSDMD pathway in BV2 cells
AU - Mei Luo
AU - Zeng-Rui Wang
AU - Xing-Ling Tan
AU - Xia Yang
AU - Zong Ning
PY - 2026
DA - 2026/07/30
JO - Cell Biology and Toxicology
DO - 10.1007/s10565-026-10240-w
UR - https://doi.org/10.1007/s10565-026-10240-w
AB - 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.
SN - 0742-2091
SN - 1573-6822
ER -