ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026
[Growth differentiation factor 11 attenuates hypoxia/reoxygenation injury in rat H9C2 cardiomyocytes
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo verify the hypothesis that growth differentiation factor 11 (GDF11) attenuates myocardial ischemia/reperfusion (MI/R) injury and explore the underlying mechanism.
methodsTo simulate MI/R injury, H9C2 cells were incubated in an anaerobic chamber (95% N
resultsIn H9C2 cells with H/R exposure, 10 nmol/L GDF11 treatment significantly increased cell viability, decreased LDH release, inhibited caspase-3 activation and cell apoptosis, and reduced superoxide production, total NO content and nitrotyrosine production. GDF11 also significantly inhibited iNOS expression, reversed H/R-induced increase of Trx1 nitration and inhibition of Trx1 activity, and inhibited ASK1 phosphorylation. Treatment of the cells with 1400W decreased LDH release and caspase-3 activity, and diminished total NO production and nitrotyrosine production. EUK134 diminished LDH release and caspase-3 activation, upregulated Trx activity, and inhibited superoxide production in H9C2 cells. N-Trx1 abolished the protective effects of GDF11 against H/R injury in the cardiomyocytes.
conclusionsGDF11 protects cardiomyocytes against H/R injury partially by attenuating oxidative/nitrative stress and inhibiting Trx1 nitrative inactivation.
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