Resveratrol protects H9c2 cells against hypoxia-induced apoptosis through miR-30d-5p/SIRT1/NF-κB axis

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dc.contributor.authorHan, Xiaen_US
dc.contributor.authorZhang, Luen_US
dc.contributor.authorLiu, Yingcaien_US
dc.contributor.authorWu, Menghaien_US
dc.contributor.authorLi, Xingchaoen_US
dc.contributor.authorZhang, Zeng Tangen_US
dc.contributor.authorLi, Taoen_US
dc.date.accessioned2020-11-18T10:14:22Z
dc.date.available2020-11-18T10:14:22Z
dc.date.issued2020-02
dc.description.abstractPrevious studies have demonstrated the cardioprotective role of resveratrol (Res). However, the underlyingmolecular mechanisms involved in the protective role of Res are still largely unknown. H9c2 cells weredistributed into five groups: normal condition (Control), DMSO, 20 mMRes (dissolved with DMSO), hypoxia(Hyp), and Res?Hyp. Cell apoptosis was evaluated using flow cytometry and protein analysis of cleavedcaspase 3 (cle-caspase 3). qRT-PCR assay was performed to measure the expression of microRNA-30d-5p(miR-30d-5p). MTT assay was performed to evaluate the cell proliferation. The relationship between miR-30d5p and silent information regulator 1 (SIRT1) was confirmed by luciferase reporter, RNA immunoprecipitation(RIP), and western blot assays. Western blot was performed to analyze NF-jB/p65 and I-jBa expressions. Ourdata showed that hypoxia enhanced apoptosis and NF-jB signaling pathway, which was alleviated by Restreatment. Hypoxia increased the expression of miR-30d-5p while decreased the SIRT1expression, which wasalso attenuated by Res treatment. Furthermore, miR-30d-5p depletion inhibited the proliferation, reducedapoptosis and decreased the expression of cle-caspase 3 in H9c2 cells with hypoxia treatment. Luciferasereporter, RIP, and western blot assays further confirmed that miR-30d-5p negatively regulated the expression ofSIRT1. Interestingly, the rescue-of-function experiments further indicated that knockdown of SIRT1 attenuatedthe effect of miR-30d-5p depletion on proliferation, apoptosis NF-jB signaling pathway inH9c2 cells withhypoxia treatment. In addition, the suppression of NF-jB signaling pathway increased cell viability whiledecreased cell apoptosis in hypoxia-mediatedH9c2 cells. Our data suggested Res mayprotectH9c2 cells againsthypoxia-induced apoptosis through miR-30d-5p/SIRT1/NF-jB axisen_US
dc.identifier.affiliationsDepartment of Cardiology, Jinan City People’s Hospital, Jinan, Chinaen_US
dc.identifier.affiliationsDepartment of Medicine, Laiwu People’s Hospital of Jinan, Laiwu, Chinaen_US
dc.identifier.affiliationsDepartment of Acupuncture, Jinan City People’s Hospital, Jinan, Chinaen_US
dc.identifier.affiliationsDepartment of Neurology, Jinan City People’s Hospital, Jinan, Chinaen_US
dc.identifier.affiliationsDepartment of Pediatrics, Taihe Hospital, Hubei University of Medicine, Hubei, Chinaen_US
dc.identifier.affiliationsDepartment of Cardiology, Jinan City People’s Hospital, Jinan, Chinaen_US
dc.identifier.affiliationsDepartment of Pediatrics, Taihe Hospital, Hubei University of Medicine, Hubei, Chinaen_US
dc.identifier.citationHan Xia, Zhang Lu, Liu Yingcai, Wu Menghai, Li Xingchao, Zhang Zeng Tang, Li Tao. Resveratrol protects H9c2 cells against hypoxia-induced apoptosis through miR-30d-5p/SIRT1/NF-κB axis. Journal of Biosciences. 2020 Feb; : 1-10en_US
dc.identifier.issn0250-5991
dc.identifier.issn0973-7138
dc.identifier.placeIndiaen_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/214322
dc.languageenen_US
dc.publisherIndian Academy of Sciencesen_US
dc.relation.volume45en_US
dc.source.urihttps://dx.doi.org//10.1007/s12038-020-9997-9en_US
dc.subjectApoptosisen_US
dc.subjecthypoxiaen_US
dc.subjectmiR-30d-5p/SIRT1/NF-jB axisen_US
dc.subjectresveratrolen_US
dc.titleResveratrol protects H9c2 cells against hypoxia-induced apoptosis through miR-30d-5p/SIRT1/NF-κB axisen_US
dc.typeJournal Articleen_US
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