6-Formylindolo[3,2-b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial-dependent manner

文献类型： 外文期刊

第一作者： Gan, Min

作者： Gan, Min;Ding, Hongbiao;Gan, Min;Ding, Hongbiao;Chen, Gang

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关键词： 6-formylindolo[3; 2-b]carbazole; AhR pathway; apoptosis; benzo[a]pyrene; proliferation

期刊名称：CELL BIOLOGY INTERNATIONAL （ 影响因子：3.612； 五年影响因子：3.055 ）

ISSN： 1065-6995

年卷期： 2020 年 44 卷 12 期

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收录情况： SCI

摘要： Benzo[a]pyrene (B[a]P), a potent carcinogen, has been proved that it can induce apoptosis via activation of the aryl hydrocarbon receptor (AhR) pathway. The metabolite of tryptophan 6-formylindolo[3,2-b]carbazole (FICZ), an endogenous activator of AhR, plays bifunctional roles in cell growth and apoptosis. However, whether and how FICZ can reduce the toxicity of B[a]P and the mechanism underlying this remain unclear. In this study, FICZ interfered with the toxicity of B[a]P in mouse hepatocarcinoma cell line Hepa1-6. The results of the MTT assay indicated that FICZ and B[a]P made opposite effects on cell proliferation. The scratch-wound healing assay showed that B[a]P (1 mu M for 24 hr) exposure triggered cell migration and that was inhibited by FICZ (10 nM). In addition, FICZ ameliorated B[a]P-induced apoptosis by inhibiting reactive oxygen species generation and caspase-3 activation, as well as increasing reduced glutathione level in mitochondria. Furthermore, gene expression analyses indicated that FICZ competed with B[a]P, which reduced the transcriptional activation of thecyp1a1andcyp1b1genes, as well asBcl2andP53. Accordingly, the interaction between FICZ and B[a]P in the AhR pathway inhibited apoptosis in a mitochondrial-dependent manner, suggesting that endogenous compound may reduce the toxicity of exogenous pollutant in vivo and providing an available way to improve health condition related to the hepatic metabolic disorder.

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