PMID- 32148653 OWN - NLM STAT- MEDLINE DCOM- 20201019 LR - 20211204 IS - 1942-0994 (Electronic) IS - 1942-0900 (Print) IS - 1942-0994 (Linking) VI - 2020 DP - 2020 TI - Autophagy Triggered by Oxidative Stress Appears to Be Mediated by the AKT/mTOR Signaling Pathway in the Liver of Sleep-Deprived Rats. PG - 6181630 LID - 10.1155/2020/6181630 [doi] LID - 6181630 AB - Sleep deprivation adversely affects the digestive system. Multiple studies have suggested sleep deprivation and oxidative stress are closely related. Autophagy can be triggered by oxidative stress as a self-defense strategy to promote survival. In this study, we investigated the effects of sleep deprivation on liver functions, oxidative stress, and concomitant hepatocyte autophagy, as well as the associated pathways. Enzymatic and nonenzymatic biochemical markers in the serum were used to assess hepatic function and damage. To evaluate the occurrence of autophagy, expression of autophagy-related proteins was tested and autophagosomes were labeled. Additionally, methane dicarboxylic aldehyde (MDA), antioxidant enzymes, and the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway were analyzed using chemical methods and a Western blot. Serum alanine transaminase, aspartate aminotransferase, and alkaline phosphatase increased in sleep-deprived rats. Total protein and albumin abundance was also abnormal. Sleep deprivation induced histopathological changes in the liver. The superoxide dismutase level decreased significantly in the liver of sleep-deprived rats. In contrast, the MDA content increased in the sleep deprivation group. Moreover, the microtubule-associated protein 1 light chain 3 beta (LC3B) II/I ratio and Beclin I content increased considerably in the sleep-deprived rats, while p62 levels decreased. Sleep deprivation apparently inhibited the AKT/mTOR signaling pathway. We conclude that sleep deprivation can induce oxidative stress and ultimately cause liver injury. Autophagy triggered by oxidative stress appears to be mediated by the AKT/mTOR pathway and plays a role in relieving oxidative stress caused by sleep deprivation. CI - Copyright (c) 2020 Yongmei Li et al. FAU - Li, Yongmei AU - Li Y AUID- ORCID: 0000-0003-1808-6060 AD - NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China. FAU - Zhang, Yuan AU - Zhang Y AUID- ORCID: 0000-0002-5019-8911 AD - Basic Medical College, Tianjin Medical University, Tianjin, China. FAU - Ji, Guang AU - Ji G AUID- ORCID: 0000-0002-6349-5114 AD - NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China. FAU - Shen, Yiwei AU - Shen Y AD - Basic Medical College, Tianjin Medical University, Tianjin, China. FAU - Zhao, Nan AU - Zhao N AD - NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China. FAU - Liang, Yuhan AU - Liang Y AD - Basic Medical College, Tianjin Medical University, Tianjin, China. FAU - Wang, Zihan AU - Wang Z AUID- ORCID: 0000-0001-8193-7054 AD - Basic Medical College, Tianjin Medical University, Tianjin, China. FAU - Liu, Mengqi AU - Liu M AD - Basic Medical College, Tianjin Medical University, Tianjin, China. FAU - Lin, Laixiang AU - Lin L AUID- ORCID: 0000-0002-0100-4084 AD - NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China. AD - Qinghai Institute for Endemic Disease Prevention and Control, Qinghai, China. LA - eng PT - Journal Article DEP - 20200213 PL - United States TA - Oxid Med Cell Longev JT - Oxidative medicine and cellular longevity JID - 101479826 RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Animals MH - Autophagy MH - Liver/*physiopathology MH - Male MH - Proto-Oncogene Proteins c-akt/*metabolism MH - Rats MH - Rats, Wistar MH - Signal Transduction MH - Sleep Deprivation/*complications MH - TOR Serine-Threonine Kinases/*metabolism PMC - PMC7044486 COIS- The authors declare that there is no conflict of interests regarding the publication of this article. EDAT- 2020/03/10 06:00 MHDA- 2020/10/21 06:00 PMCR- 2020/02/13 CRDT- 2020/03/10 06:00 PHST- 2019/04/04 00:00 [received] PHST- 2019/10/22 00:00 [revised] PHST- 2019/12/11 00:00 [accepted] PHST- 2020/03/10 06:00 [entrez] PHST- 2020/03/10 06:00 [pubmed] PHST- 2020/10/21 06:00 [medline] PHST- 2020/02/13 00:00 [pmc-release] AID - 10.1155/2020/6181630 [doi] PST - epublish SO - Oxid Med Cell Longev. 2020 Feb 13;2020:6181630. doi: 10.1155/2020/6181630. eCollection 2020.