Abstract:
:Mycobacterium tuberculosis (MTB) infection can induce cytotoxicity to the host macrophages, promoting bacterial spread. We here tested the potential effect of oltipraz, a synthetic dithiolethione, in MTB-infected human macrophages. We show that oltipraz significantly inhibited MTB-induced death and apoptosis in human macrophages. MTB-induced reactive oxygen species production, mitochondrial depolarization and programmed necrosis were attenuated by oltipraz in macrophages. Oltipraz activated Nrf2 signaling, causing Keap1-Nrf2 disassociation, Nrf2 protein stabilization and nuclear translocation, simultaneously promoting expression of Nrf2-dependent genes (HO1, NQO1 and GST) in human macrophages. Nrf2 shRNA or CRISPR/Cas9-induced Nrf2 knockout completely reversed oltipraz-induced macrophage protection against MTB infection. Furthermore, CRISPR/Cas9-mediated Keap1 knockout induced Nrf2 cascade activation and protected human macrophages from MTB. Importantly, oltipraz was unable to offer further cytoprotection against MTB in Keap1 knockout macrophages. Collectively we conclude that oltipraz activates Nrf2 signaling cascade to protect human macrophages from MTB-induced oxidative injury and cell death.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Sun Q,Shen X,Ma J,Lou H,Zhang Qdoi
10.1016/j.bbrc.2020.07.026subject
Has Abstractpub_date
2020-10-20 00:00:00pages
312-319issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)31413-3journal_volume
531pub_type
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