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Archives of Physiology and Biochemistry
The Journal of Metabolic Diseases
Volume 130, 2024 - Issue 1
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Original Articles

Phoenixin-14 protects cardiac damages in a streptozotocin-induced diabetes mice model through SIRT3

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Pages 110-118 | Received 18 Jun 2021, Accepted 13 Sep 2021, Published online: 07 Oct 2021
 

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.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions

Bo Yao and Zhao Xu made substantial contributions to the concepts of the study; Bo Yao, Junlin Lv, Le Du, and Hui Zhang made contributions to the methodology, investigation, and data analysis; Zhao Xu drafted the manuscript. All authors have read and approved the final submission.

Data availability statement

Experimental data are available based on a reasonable request to the corresponding author.

Additional information

Funding

This study is funded by “Xi'an Jiaotong University.”

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