Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Hongrui Guo; Huan Liu; Zhijie Jian; Hengmin Cui; Jing Fang; Zhicai Zuo; Junliang Deng; Yinglun Li; Xun Wang; Ling Zhao; Yi Geng; Ping Ouyang; Weiming Lai; Zhengli Chen; Chao Huang

doi:doi:10.18632/aging.102570

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Research Paper Volume 11, Issue 23 pp 11659—11672

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Figure 6. NiCl₂ induces apoptosis in BMDMs. (A and B) Immunoblot analysis of cleaved-caspase-8, cleaved-caspase-9, cleaved-caspase-3 and cleaved-PARP in lysates of the NiCl₂-treated BMDMs. (C) Immunoblot analysis of pro-caspase-1, cleaved-caspase-1, pro-IL-1β, cleaved- IL-1β, NLRP3, ASC and cleaved-caspase-3 in the NiCl₂-treated (24h) BMDMs in the presence/absence of Mito-TEMPO (500 μM, 1h) or Z-YVAD-FMK (100 μM, 1h) pre-treatment, and cleaved-caspase-1and cleaved- IL-1β in the supernatant. (D) Flow cytometry analysis apoptosis in the NiCl₂-treated (24h) BMDMs in the presence/absence of Mito-TEMPO (500 μM, 1h) or Z-YVAD-FMK (100 μM, 1h) pre-treatment. Data are presented with the means ± standard deviation (n=5). *p < 0.05 and **p < 0.01, compared with the control group.