Souza Lidiane Moreira, Damatto Felipe Cesar, Brandão Bruna Brasil, Rodrigues Eder Anderson, Santos Anna Clara Consorti, Silva Rafael Campos França, Gatto Mariana, Pagan Luana Urbano, Martinez Paula Felippe, Murata Gilson Masahiro, Zornoff Leonardo Antonio Mamede, Gaiolla Paula Schmidt Azevedo, Falcão-Pires Inês, Okoshi Katashi, Okoshi Marina Politi
Department of Internal Medicine, Botucatu Medical School, Sao Paulo State University-UNESP, Botucatu 18618-687, Brazil.
Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02115, USA.
Antioxidants (Basel). 2025 May 28;14(6):647. doi: 10.3390/antiox14060647.
Skeletal muscle changes occur in heart failure (HF). Despite the cardioprotective effects of sodium-glucose co-transporter 2 (SGLT2) inhibitors in HF, their impact on skeletal muscle remains poorly understood. We investigated the effects of the SGLT2 inhibitor empagliflozin (EMPA) on cardiac remodeling and the soleus muscle of rats with myocardial infarction (MI)-induced HF.
One week after MI induction, rats were assigned to Sham, Sham + EMPA, MI, and MI + EMPA groups. EMPA was administered (5 mg/kg/day) for 12 weeks.
MI + EMPA and MI had dilated left cardiac chambers; the left atrium diameter and left ventricle end-diastolic area were smaller in MI + EMPA than MI. The ejection fraction did not differ between infarcted groups. MI + EMPA had a larger soleus cross-sectional area and higher Type II myosin heavy chain expression than MI. Carbonylated protein and malondialdehyde levels were lower and superoxide dismutase activity higher in MI + EMPA than MI. Respiratory Complex I expression was higher in MI + EMPA than MI. Metabolic enzyme activities, altered in MI, were normalized in MI + EMPA. EMPA up-regulated anabolic proteins and down-regulated catabolic proteins.
Empagliflozin attenuates infarction-induced cardiac remodeling in rats. In soleus muscle, empagliflozin preserves cell trophism, reduces oxidative stress, normalizes muscle and mitochondrial metabolism, and positively modulates proteins involved in synthesis and degradation-related pathways.
心力衰竭（HF）时会发生骨骼肌变化。尽管钠-葡萄糖协同转运蛋白2（SGLT2）抑制剂在HF中具有心脏保护作用，但其对骨骼肌的影响仍知之甚少。我们研究了SGLT2抑制剂恩格列净（EMPA）对心肌梗死（MI）诱导的HF大鼠心脏重塑和比目鱼肌的影响。
MI诱导1周后，将大鼠分为假手术组、假手术+EMPA组、MI组和MI+EMPA组。给予EMPA（5mg/kg/天），持续12周。
MI+EMPA组和MI组左心腔扩张；MI+EMPA组的左心房直径和左心室舒张末期面积小于MI组。梗死组间射血分数无差异。MI+EMPA组比目鱼肌横截面积更大，II型肌球蛋白重链表达更高。MI+EMPA组羰基化蛋白和丙二醛水平低于MI组，超氧化物歧化酶活性高于MI组。MI+EMPA组呼吸复合体I表达高于MI组。MI中改变的代谢酶活性在MI+EMPA组中恢复正常。EMPA上调合成代谢蛋白，下调分解代谢蛋白。
恩格列净减轻大鼠梗死诱导的心脏重塑。在比目鱼肌中，恩格列净可维持细胞营养，减少氧化应激，使肌肉和线粒体代谢正常化，并积极调节参与合成和降解相关途径的蛋白质。
