Bo Yao1, Junlin Lv2, Le Du1, Hui Zhang1, Zhao Xu1. 1. Department of Anesthesiology, Shaanxi Provincial People's Hospital, Third Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China. 2. Department of Anesthesiology, The Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Abstract
BACKGROUND: Type I diabetes is a metabolic syndrome that severely impacts the normal lives of patients through its multiple complications, such as diabetic cardiomyopathy (DCM). Phoenixin-14 is a peptide found to be widely expressed in eukaryons with multiple protective properties, including anti-oxidative stress and anti-inflammatory effects. The present study aims to explore the potential therapeutic impacts of Phoenixin-14 on DCM. METHODS: Type I diabetes was induced by treatment with a single dose of STZ (40 mg/kg body weight) intraperitoneally for 5 consecutive days. Mice were divided into four groups: the Control, Phoenixin-14, T1DM, and Phoenixin-14 +T1DM groups. The levels of myocardial injury markers were measured. Cardiac hypertrophy was assessed using wheat germ agglutinin (WGA) staining. RESULTS: Phoenixin-14 was significantly downregulated in the cardiac tissue of diabetic mice. The myocardial injury and deteriorated cardiac function in diabetic mice induced by STZ were significantly ameliorated by Phoenixin-14, accompanied by the alleviation of cardiac hypertrophy. In addition, the severe oxidative stress and inflammation in diabetic mice were dramatically mitigated by Phoenixin-14. Lastly, the downregulated SIRT3 and upregulated p-FOXO3 in diabetic mice were pronouncedly reversed by Phoenixin-14. It is worth mentioning that compared to the Control, no significant changes to any of the investigated parameters in the present study were found in the Phoenixin-14-treated normal mice, suggesting that treatment with it has no side effects. CONCLUSION: Our data revealed that Phoenixin-14 protected against cardiac damages in STZ-induced diabetes mice models.
BACKGROUND: Type I diabetes is a metabolic syndrome that severely impacts the normal lives of patients through its multiple complications, such as diabetic cardiomyopathy (DCM). Phoenixin-14 is a peptide found to be widely expressed in eukaryons with multiple protective properties, including anti-oxidative stress and anti-inflammatory effects. The present study aims to explore the potential therapeutic impacts of Phoenixin-14 on DCM. METHODS: Type I diabetes was induced by treatment with a single dose of STZ (40 mg/kg body weight) intraperitoneally for 5 consecutive days. Mice were divided into four groups: the Control, Phoenixin-14, T1DM, and Phoenixin-14 +T1DM groups. The levels of myocardial injury markers were measured. Cardiac hypertrophy was assessed using wheat germ agglutinin (WGA) staining. RESULTS: Phoenixin-14 was significantly downregulated in the cardiac tissue of diabetic mice. The myocardial injury and deteriorated cardiac function in diabetic mice induced by STZ were significantly ameliorated by Phoenixin-14, accompanied by the alleviation of cardiac hypertrophy. In addition, the severe oxidative stress and inflammation in diabetic mice were dramatically mitigated by Phoenixin-14. Lastly, the downregulated SIRT3 and upregulated p-FOXO3 in diabetic mice were pronouncedly reversed by Phoenixin-14. It is worth mentioning that compared to the Control, no significant changes to any of the investigated parameters in the present study were found in the Phoenixin-14-treated normal mice, suggesting that treatment with it has no side effects. CONCLUSION: Our data revealed that Phoenixin-14 protected against cardiac damages in STZ-induced diabetes mice models.