<p>L-Tartaric acid is a white, crystalline organic acid commonly found in fruit, particularly grapes. The cardio-protective effects of L-Tartaric acid have been previously reported in multiple studies, but its effect on diabetic cardiomyopathy and its correlation with autophagy, apoptosis, and inflammation is still unclear. The purpose of the present study was to explore how L-Tartaric acid could be beneficial against cardiac failure in mice with diabetes. Diabetes in mice was induced with streptozotocin (STZ) to establish a diabetic cardiomyopathy model. After 16 weeks of oral administration of L-Tartaric acid at doses of 50 and 100&#xa0;mg/kg, cardiac function tests were performed to evaluate the effect of treatment, and autophagy, apoptosis, inflammation, and oxidative stress markers were assessed at mRNA as well as protein levels. The diabetic mice that received long-term treatment with L-Tartaric acid showed improved cardiac function, improved oxidative damage, and decreased apoptosis in their hearts. Furthermore, the study indicated that L-Tartaric acid was associated with increased levels of autophagy-related proteins. These results highlight the potential therapeutic benefits of L-Tartaric acid as a possible way for managing diabetic cardiomyopathy.</p>

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l-Tartaric acid mitigates diabetic cardiac damage and is associated with changes in autophagy, apoptosis, and inflammatory markers

  • Weigang Chen,
  • Ming Lin,
  • Kun Yan,
  • Jie Gao,
  • Nehmar Poudi,
  • Zhao Gao

摘要

L-Tartaric acid is a white, crystalline organic acid commonly found in fruit, particularly grapes. The cardio-protective effects of L-Tartaric acid have been previously reported in multiple studies, but its effect on diabetic cardiomyopathy and its correlation with autophagy, apoptosis, and inflammation is still unclear. The purpose of the present study was to explore how L-Tartaric acid could be beneficial against cardiac failure in mice with diabetes. Diabetes in mice was induced with streptozotocin (STZ) to establish a diabetic cardiomyopathy model. After 16 weeks of oral administration of L-Tartaric acid at doses of 50 and 100 mg/kg, cardiac function tests were performed to evaluate the effect of treatment, and autophagy, apoptosis, inflammation, and oxidative stress markers were assessed at mRNA as well as protein levels. The diabetic mice that received long-term treatment with L-Tartaric acid showed improved cardiac function, improved oxidative damage, and decreased apoptosis in their hearts. Furthermore, the study indicated that L-Tartaric acid was associated with increased levels of autophagy-related proteins. These results highlight the potential therapeutic benefits of L-Tartaric acid as a possible way for managing diabetic cardiomyopathy.