Coenzyme Q0, a quinone derivative from Antrodia camphorata, triggered ROS-mediated cytoprotective autophagy in human promyelocytic leukemia cells

IF 4 2区农林科学 Q2 FOOD SCIENCE & TECHNOLOGY

Journal of Functional Foods Pub Date : 2025-06-17 DOI:10.1016/j.jff.2025.106939

Hsin-Ling Yang , Pei-Yuan Chiu , Hui-Jye Chen , Sudhir Pandey , Yue-Tong Chen , Siang-Jyun Chen , Yu-Lyu Yeh , Hsueh-Wei Chang , Jhih-Hsuan Hseu , You-Cheng Hseu

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引用次数: 0

Abstract

Our previous investigation revealed that Coenzyme Q₀ (CoQ₀), a quinone derivative from Antrodia camphorata, triggered ROS-dependent voltage-dependent anion channel 1 (VDAC-1)-mediated apoptosis in human promyelocytic leukemia (HL-60) cells. This research examined the efficacies of CoQ₀ (0–7 μM) on autophagy induction and the interaction between apoptosis and autophagy in HL-60 cells. CoQ₀-triggered autophagy was associated with LC3-I/II accumulation, p62/SQSTM1 activation, autolysosome AVOs formation, ATG4B inhibition, ATG5/ATG7 expression, and Beclin-1/Bcl-2 dysregulation in HL-60 cells. Additionally, antioxidant N-acetylcysteine (NAC) prevented CoQ₀-induced autophagy in HL-60 cells. Surprisingly, CoQ₀-triggered cell death was enhanced by autophagy inhibitor 3-MA or CQ, indicating that autophagy acts as a survival mechanism. Additionally, autophagy suppression via 3-MA and/or CQ inhibitors strengthened the CoQ₀-induced ROS generation and apoptosis (caspase-3 activation). Apoptosis suppression by caspase inhibitor Z-VAD-FMK or VDAC-1 silencing prevented the CoQ₀-enhanced autophagy in HL-60 cells. Therefore, CoQ₀ together with autophagy inhibitors could be a potential therapy for human promyelocytic leukemia.

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辅酶Q0是一种从樟树中提取的醌衍生物，在人早幼粒细胞白血病细胞中引发ros介导的细胞保护性自噬

我们之前的研究发现，辅酶Q0 （CoQ0）是一种从香樟中提取的醌衍生物，可触发ros依赖性电压依赖性阴离子通道1 （VDAC-1）介导的人早幼粒细胞白血病（HL-60）细胞凋亡。本研究考察了辅酶q0 （0-7 μM）诱导HL-60细胞自噬的作用及凋亡与自噬的相互作用。在HL-60细胞中，coq0触发的自噬与LC3-I/II积累、p62/SQSTM1激活、自溶酶体AVOs形成、ATG4B抑制、ATG5/ATG7表达和Beclin-1/Bcl-2失调有关。此外，抗氧化剂n -乙酰半胱氨酸（NAC）可阻止coq0诱导的HL-60细胞自噬。令人惊讶的是，自噬抑制剂3-MA或CQ可增强coq0触发的细胞死亡，表明自噬是一种生存机制。此外，通过3-MA和/或CQ抑制剂抑制自噬增强了coq0诱导的ROS生成和凋亡（caspase-3激活）。caspase抑制剂Z-VAD-FMK或VDAC-1沉默抑制HL-60细胞的凋亡，可阻止coq0增强的自噬。因此，CoQ0联合自噬抑制剂可能是人类早幼粒细胞白血病的潜在治疗方法。

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来源期刊

Journal of Functional Foods FOOD SCIENCE & TECHNOLOGY-

CiteScore

9.60

自引率

1.80%

发文量

428

审稿时长

76 days

期刊介绍： Journal of Functional Foods continues with the same aims and scope, editorial team, submission system and rigorous peer review. We give authors the possibility to publish their top-quality papers in a well-established leading journal in the food and nutrition fields. The Journal will keep its rigorous criteria to screen high impact research addressing relevant scientific topics and performed by sound methodologies. The Journal of Functional Foods aims to bring together the results of fundamental and applied research into healthy foods and biologically active food ingredients. The Journal is centered in the specific area at the boundaries among food technology, nutrition and health welcoming papers having a good interdisciplinary approach. The Journal will cover the fields of plant bioactives; dietary fibre, probiotics; functional lipids; bioactive peptides; vitamins, minerals and botanicals and other dietary supplements. Nutritional and technological aspects related to the development of functional foods and beverages are of core interest to the journal. Experimental works dealing with food digestion, bioavailability of food bioactives and on the mechanisms by which foods and their components are able to modulate physiological parameters connected with disease prevention are of particular interest as well as those dealing with personalized nutrition and nutritional needs in pathological subjects.