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Activation of APE1 modulates Nrf2 protected against acute liver injury by inhibit hepatocyte ferroptosis and promote hepatocyte autophagy

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Pubmed体系：

收录情况： ◇ SCIE

作者：
Diao Jianxin[1,2] * ; Fan Huijie[2,3] * ; Zhang Jia[2] * ; Fu Xiuqiong[4] * ; Liao Rongxin[1] ; Zhao Peng[1] ; Huang Wei[1] ; Huang Shiying[2] ; Liao Huajun[2] ; Yu Jieying[2] ; Pan Dongmei[2] ; Wang Ming[2,5,*1] ; Xiao Wei[2,6,*1] ; Wen Xiaomin[1,2,*1] ;
机构： [1]Center of TCM Preventive Treatment, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China [3]Department of Traditional Chinese Medicine, People’s Hospital of Yangjiang, Yangjiang 529500, China [4]School of Chinese Medicine, Consun Chinese Medicines Research Centre for Renal Diseases, Hong Kong Baptist University, Hong Kong, China [5]Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510515, China [6]Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China
出处：
DOI： 10.1016/j.intimp.2024.111529
ISSN：

关键词： Acute liver injury Apurinic/apyrimidinic endonuclease 1/redox effector factor 1 Ferroptosis Autophagy Nuclear erythroid factor 2 like 2

摘要：
Apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APE1/Ref-1) plays a crucial role in DNA base excision repair, cell apoptosis, cell signaling, and the regulation of transcription factors through redox modulation and the control of reactive oxygen species (ROS). However, the connection between APE1 and acute liver injury (ALI) remains enigmatic. This study aims to unravel the molecular mechanisms underlying ALI and shed light on the role of APE1 in this context.We induced acute liver injury (ALI) in mice by lipopolysaccharide/D-galactosamine (LPS/GalN) and intervened with the APE1 inhibitor E3330. We examined the expression of APE1 in ALI mice and ALI patient tissues after E3330 intervention, Additionally, we measured hepatic oxidative stress, ferroptosis, and autophagy marker proteins and genes. In establishing an AML-12 liver cell injury model, we utilized the Nrf2 activator tert-butylhydroquinone (TBHQ) as an intervention and examined APE1, Nrf2, ferroptosis-related proteins, and autophagy marker proteins and mRNA.Both ALI patients and ALI mice exhibited reduced APE1 expression levels. After E3330 intervention, there was a significant exacerbation of liver injury, oxidative stress, and a reduction in the expression of proteins, including GPX4, X-CT, ATG3, ATG5, and LC3 (LC3I/II). Consistent results were also observed in AML-12 cells. With TBHQ intervention, Nrf2 expression increased, along with the expression of proteins associated with iron death and autophagy. Mechanistically, APE1 activation regulates Nrf2 to inhibit ferroptosis and promote autophagy in hepatocytes.The data suggest that APE1 is a pivotal player in ALI, closely linked to its regulation of Nrf2. Strategies involving APE1 activation to modulate Nrf2, thereby inhibiting hepatocyte ferroptosis and promoting autophagy, may represent innovative therapeutic approaches for ALI. Additionally, tert-butylhydroquinone (TBHQ) holds significant promise in the treatment of acute liver injury.Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.

基金：
This work was supported by the National Natural Science Foundation of China (No. 82074257, 82174323 and 82004103), the Natural Science Foundation of Guangdong Province (2019A1515011034, 2023A1515011200 and 2022A1515011668), the Project of Administration of Traditional Chinese Medicine of Guangdong Province (20232068) and the Scientific Research Fund of People’s Hospital of Yangjiang (No. G2020001).
语种：
外文
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2023]版：
大类 | 2 区 医学
小类 | 2 区 免疫学 2 区 药学
最新[2025]版：
大类 | 2 区 医学
小类 | 2 区 药学 3 区 免疫学
JCR分区：
出版当年[2022]版：
Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2022版] 出版当年五年平均 出版前一年[2021版] 出版后一年[2023版]

第一作者：
第一作者机构： [1]Center of TCM Preventive Treatment, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China
共同第一作者：
通讯作者：
通讯机构： [1]Center of TCM Preventive Treatment, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China [2]School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China [5]Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510515, China [6]Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China [*1]Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China.
推荐引用方式(GB/T 7714)：
Diao Jianxin,Fan Huijie,Zhang Jia,et al.Activation of APE1 modulates Nrf2 protected against acute liver injury by inhibit hepatocyte ferroptosis and promote hepatocyte autophagy[J].INTERNATIONAL IMMUNOPHARMACOLOGY.2024,128:111529.doi:10.1016/j.intimp.2024.111529.
APA：
Diao Jianxin,Fan Huijie,Zhang Jia,Fu Xiuqiong,Liao Rongxin...&Wen Xiaomin.(2024).Activation of APE1 modulates Nrf2 protected against acute liver injury by inhibit hepatocyte ferroptosis and promote hepatocyte autophagy.INTERNATIONAL IMMUNOPHARMACOLOGY,128,
MLA：
Diao Jianxin,et al."Activation of APE1 modulates Nrf2 protected against acute liver injury by inhibit hepatocyte ferroptosis and promote hepatocyte autophagy".INTERNATIONAL IMMUNOPHARMACOLOGY 128.(2024):111529

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