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      Dihydromyricetin protects HUVECs of oxidative damage induced by sodium nitroprusside through activating PI3K/Akt/FoxO3a signalling pathway

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          Abstract

          The damage of vascular endothelial cells induced by oxidative stress plays an important role in the pathogenesis of atherosclerosis. Dihydromyricetin (DMY) is considered as a natural antioxidant. However, the mechanism of DMY on endothelial cell injury induced by oxidative stress remains unclear. In this study, we found that DMY could reduce the oxidative damage of HUVECs induced by sodium nitroprusside (SNP), HUVECs pre‐treated with DMY suppressed SNP‐induced apoptosis by reduced ROS overproduction of intracellular, decreased MDA level and elevated the superoxide dismutase activity. Meanwhile, we found that DMY could promote the expression of phosphorylated FoxO3a and Akt, and affect the nuclear localization of FoxO3a, when treated with the PI3K inhibitor LY294002, the effect of DMY was blocked. These data suggest that DMY protects HUVECs from oxidative stress by activating PI3K/Akt/FoxO3a signalling pathway. Therefore, DMY may have great therapeutic potential as a new drug for atherosclerosis.

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          Functional interaction between beta-catenin and FOXO in oxidative stress signaling.

          Marieke Essers, Lydia M M de Vries-Smits, Nick Barker … (2005)
          beta-Catenin is a multifunctional protein that mediates Wnt signaling by binding to members of the T cell factor (TCF) family of transcription factors. Here, we report an evolutionarily conserved interaction of beta-catenin with FOXO transcription factors, which are regulated by insulin and oxidative stress signaling. beta-Catenin binds directly to FOXO and enhances FOXO transcriptional activity in mammalian cells. In Caenorhabditis elegans, loss of the beta-catenin BAR-1 reduces the activity of the FOXO ortholog DAF-16 in dauer formation and life span. Association of beta-catenin with FOXO was enhanced in cells exposed to oxidative stress. Furthermore, BAR-1 was required for the oxidative stress-induced expression of the DAF-16 target gene sod-3 and for resistance to oxidative damage. These results demonstrate a role for beta-catenin in regulating FOXO function that is particularly important under conditions of oxidative stress.
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            Forkhead homeobox type O transcription factors in the responses to oxidative stress.

            Peter Storz (2011)
            Reactive oxygen species (ROS) and cellular oxidative stress are involved in many physiological and pathophysiological processes, including cellular and organismal aging, migration, proliferation, senescence or death of normal and cancer cells, and stress resistance of stem cells. The forkhead homeobox type O (FOXO) transcription factors FOXO1, FOXO3a, and FOXO4 are critical mediators of the cellular responses to oxidative stress and have been implicated in many of the above ROS-regulated processes. In cancer cells they converge oxidative stress signaling to cell cycle arrest and cell death or promote a motile phenotype. Dependent on their posttranslational modifications FOXOs can also actively regulate the detoxification of cells from ROS and promote stress resistance. Thus, FOXO transcription factors are of vital importance in processes regulating tumor survival or progression, stem cell maintenance, age-related pathological processes, and lifespan extension.
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              Dihydromyricetin inhibits NLRP3 inflammasome-dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells: Nrf2 Signaling Pathway in Vascular Endothelial Cells

              Qin Hu, Ting Zhang, Long Yi … (2018)
              Increasing evidence demonstrates that pyroptosis, pro-inflammatory programmed cell death, is linked to atherosclerosis; however, the underlying mechanisms remain to be elucidated. Dihydromyricetin (DHM), a natural flavonoid, was reported to exert anti-oxidative and anti-inflammatory bioactivities. However, the effect of DHM on atherosclerosis-related pyroptosis has not been studied. In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1β and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels. Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis. However, DHM pretreatment inhibited PA-induced pyroptotic cell death by increasing cell viability, decreasing LDH and IL-1β release, improving cell membrane integrity, and abolishing caspase-1 cleavage and subsequent IL-1β maturation. We also found that DHM pre-treatment remarkably reduced the levels of intracellular ROS and mtROS and activated the Nrf2 signaling pathway. Moreover, knockdown of Nrf2 by siRNA abrogated the inhibitory effects of DHM on ROS generation and subsequent PA-induced pyroptosis. Together, these results indicate that the Nrf2 signaling pathway plays a role, as least in part, in the DHM-mediated improvement in PA-induced pyroptosis in vascular endothelial cells, which implies the underlying medicinal value of DHM targeting immune/inflammatory-related diseases, such as atherosclerosis. © 2017 BioFactors, 44(2):123-136, 2018.
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                Author and article information

                Contributors
                Rifang Liao:
                ORCID: https://orcid.org/0000-0001-6454-7716
                liaorf@mail.sysu.edu.cn
                Fengxia Yan:
                ORCID: https://orcid.org/0000-0002-8091-4384
                yanfengxia0807@163.com
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 21 May 2019
                Publication date (Print): July 2019
                Volume: 23
                Issue: 7 ( doiID: 10.1111/jcmm.2019.23.issue-7 )
                Pages: 4829-4838
                Affiliations
                [ 1 ] Department of Pharmacology, School of Medicine Xizang Minzu University Xianyang China
                [ 2 ] School of Medical Science Jinan University Guangzhou China
                [ 3 ] Department of Pharmacy The Seventh Affiliated Hospital of Sun Yat‐Sen University Shenzhen China
                [ 4 ] Department of Pharmacy Sun Yat‐sen Memorial Hospital, Sun Yat‐sen University Guangzhou China
                Author notes
                [*] [* ] Correspondence

                Rifang Liao, Department of Pharmacy, Sun Yat‐sen Memorial Hospital, Sun Yat‐sen University, Guangzhou, China.

                Email: liaorf@ 123456mail.sysu.edu.cn

                Fengxia Yan, School of Medical Science, Jinan University, Guangzhou, China.

                Email: yanfengxia0807@ 123456163.com

                Author information
                https://orcid.org/0000-0001-6454-7716
                https://orcid.org/0000-0002-8091-4384
                Article
                Publisher ID: JCMM14406
                DOI: 10.1111/jcmm.14406
                PMC ID: 6584490
                PubMed ID: 31111658
                SO-VID: 3dcb7767-e9a8-4c4a-bb37-5b530755380c
                Copyright © © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 10 December 2018
                Date revision received : 21 March 2019
                Date accepted : 26 April 2019
                Page count
                Figures: 9, Tables: 0, Pages: 10, Words: 5667
                Funding
                Funded by: Traditional Chinese Medicine Bureau of Guangdong Province
                Award ID: 20191086
                Award ID: 20181067
                Award ID: 20181060
                Funded by: National Natural Science Foundation of China
                Award ID: 81770241
                Award ID: 31800819
                Award ID: 31371088
                Funded by: Guangdong Natural Science Foundation
                Award ID: 2018A0303130249
                Award ID: 2018A030313435
                Award ID: 2018A32218013
                Funded by: Jinan University
                Award ID: 201910559092
                Award ID: CX2019122
                Funded by: Natural Science Foundation of Tibet
                Award ID: 2016ZR-MQ-06
                Funded by: Xizang Minzu University
                Award ID: 18MDZ03
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id jcmm14406
                cover-date July 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.4 mode:remove_FC converted:20.06.2019

                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis,atherosclerosis,dihydromyricetin,oxidative stress,sodium nitroprusside
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: apoptosis, atherosclerosis, dihydromyricetin, oxidative stress, sodium nitroprusside

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