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dc.contributor.authorHuo, Shengqi
dc.contributor.authorShi, Wei
dc.contributor.authorMa, Haiyan
dc.contributor.authorYan, Dan
dc.contributor.authorLuo, Pengcheng
dc.contributor.authorGuo, Junyi
dc.contributor.authorLi, Chenglong
dc.contributor.authorLin, Jiayuh
dc.contributor.authorZhang, Cuntai
dc.contributor.authorLi, Sheng
dc.contributor.authorLv, Jiagao
dc.contributor.authorLin, Li
dc.date.accessioned2021-04-09T15:03:21Z
dc.date.available2021-04-09T15:03:21Z
dc.date.issued2021-03-22
dc.identifier.urihttp://hdl.handle.net/10713/15135
dc.description.abstractTransverse aortic constriction (TAC) was used to induce pressure overload-HF in C57BL/6J mice. 18 mice were randomized into three groups (Sham, TAC, and TAC+raloxifene, n = 6, respectively). Echocardiographic and histological results showed that cardiac hypertrophy, fibrosis, and left ventricular dysfunction were manifested in mice after TAC treatment of eight weeks, with aggravation of macrophage infiltration and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression in the myocardium. TAC (four and eight weeks) elevated the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) and prohibitin2 (PHB2) protein expression. Importantly, IL-6/gp130/STAT3 inhibition by raloxifene alleviated TAC-induced myocardial inflammation, cardiac remodeling, and dysfunction. In vitro, we demonstrated cellular hypertrophy with STAT3 activation and oxidative stress exacerbation could be elicited by IL-6 (25 ng/mL, 48 h) in H9c2 myoblasts. Sustained IL-6 stimulation increased intracellular reactive oxygen species, repressed mitochondrial membrane potential (MMP), decreased intracellular content of ATP, and led to decreased SOD activity, an increase in iNOS protein expression, and increased protein expression of Pink1, Parkin, and Bnip3 involving in mitophagy, all of which were reversed by raloxifene.en_US
dc.description.urihttps://doi.org/10.1155/2021/6699054en_US
dc.language.isoenen_US
dc.publisherHindawien_US
dc.relation.ispartofOxidative Medicine and Cellular Longevityen_US
dc.rightsCopyright © 2021 Shengqi Huo et al.en_US
dc.subject.meshHeart Failureen_US
dc.subject.meshRaloxifine Hydrochlorideen_US
dc.titleAlleviation of Inflammation and Oxidative Stress in Pressure Overload-Induced Cardiac Remodeling and Heart Failure via IL-6/STAT3 Inhibition by Raloxifeneen_US
dc.typeArticleen_US
dc.identifier.doi10.1155/2021/6699054
dc.identifier.pmid33824698
dc.source.volume2021
dc.source.beginpage6699054
dc.source.endpage
dc.source.countryUnited States


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