上睑下垂
THP1细胞系
程序性细胞死亡
下调和上调
劈理(地质)
细胞培养
细胞凋亡
生物
Jurkat细胞
细胞生物学
化学
免疫学
T细胞
生物化学
免疫系统
基因
古生物学
遗传学
断裂(地质)
作者
Houda Huang,Xiuzhen Li,Duoduo Zha,Hong‐Ru Lin,Lingyi Yang,Yihan Wang,Liang Xu,Linsiqi Wang,Tianhua Lei,Zhou Zhou,Xiao Yan,Hong‐Bo Xin,Mingui Fu,Yisong Qian
标识
DOI:10.1139/bcb-2022-0359
摘要
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an emerging pathogenic coronavirus, has been reported to cause excessive inflammation and dysfunction in multiple cells and organs, but the underlying mechanisms remain largely unknown. Here we showed exogenous addition of SARS-CoV-2 envelop protein (E protein) potently induced cell death in cultured cell lines, including THP-1 monocytic leukemia cells, endothelial cells, and bronchial epithelial cells, in a time- and concentration-dependent manner. SARS-CoV-2 E protein caused pyroptosis-like cell death in THP-1 and led to GSDMD cleavage. In addition, SARS-CoV-2 E protein upregulated the expression of multiple pro-inflammatory cytokines that may be attributed to activation of NF-κB, JNK and p38 signal pathways. Notably, we identified a natural compound, Ruscogenin, effectively reversed E protein-induced THP-1 death via inhibition of NLRP3 activation and GSDMD cleavage. In conclusion, these findings suggested that Ruscogenin may have beneficial effects on preventing SARS-CoV-2 E protein-induced cell death and might be a promising treatment for the complications of COVID-19.
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