Alleviates Lipopolysaccharide-Induced Neuronal Pyroptosis via Promoting BIRC3-Mediated Inactivation of NLRC4.

OBJECTIVE

Neurodegenerative disease is a common neurodegenerative disorder. () plays a neuron-protective role. This study aimed to investigate the effects of on neurodegenerative diseases.

METHODS

Cells were treated with lipopolysaccharide (LPS) to establish neurodegenerative diseases model in vivo and with strain S-PT84. Reverse transcription-quantitative PCR (RT-qPCR) was applied to determine mRNA levels. Western blot was performed to detect protein expression. Cellular behaviors were detected using Cell Counting Kit-8 (CCK-8), flow cytometry, and TdT-mediated dUTP nick-end labeling (TUNEL) assay. The interaction between baculoviral IAP repeat containing 3 (BIRC3) and NLR family CARD domain containing 4 (NLRC4) was predicted by STING and verified by western blot.

RESULT

suppressed LPS-induced pyroptosis and promoted the cell viability of neurons. Additionally, suppressed the release of proinflammatory cytokines (interleukin 1 beta (IL-1) and IL-18) and the protein expression of pyroptosis biomarkers (cleaved caspase1 (CL-CASP1) and N-terminal fragment gasdermin (GSDMD-N)). Moreover, upregulated BIRC3, which induced the inactivation of NLRC4. However, BIRC3 knockdown alleviated the effects of and induced neuronal degeneration.

CONCLUSION

may play a neuron-protective role via regulating BIRC3/NLRC4 signaling pathways. Therefore, may be a promising strategy for neurodegenerative diseases.