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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

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[Protective effect and mechanism of β-CM7 on renin angiotensin system & diabetic cardiomyopathy]

Kun Wang, Dongning Han, Yujuan Zhang

    Sheng Wu Gong Cheng Xue Bao = Chinese Journal of Biotechnology
    |July 8, 2016
    PubMed

    Insights

    Beta-cryptoxanthin methyl ether (β-CM7) protects diabetic rat heart tissue by activating the ACE2-Angiotensin-(1-7)-Mas axis. This mechanism inhibits harmful renin-angiotensin system (RAS) pathways, reducing myocardial damage.

    Area of Science:

    • Cardiovascular Science
    • Endocrinology
    • Pharmacology

    Background:

    • Diabetic cardiomyopathy involves renin-angiotensin system (RAS) dysregulation.
    • The angiotensin II (Ang II) pathway contributes to myocardial damage in diabetes.

    Purpose of the Study:

    • To investigate the protective effects of β-CM7 on the RAS in diabetic rat myocardium.
    • To elucidate the mechanism of β-CM7 in mitigating diabetic myocardial injury.

    Main Methods:

    • Divided 32 male SD rats into control, diabetic, insulin-treated, and β-CM7-treated groups.
    • Administered treatments for 30 days, followed by myocardial tissue collection.
    • Analyzed Angiotensin II (Ang II), Angiotensin-(1-7) (Ang1-7), AT1 receptor, Mas receptor, ACE, and ACE2 levels and activity.

    Main Results:

    • β-CM7 decreased Ang II and increased Ang1-7 levels.
    • Improved mRNA expression of AT1 receptor, Mas receptor, ACE, and ACE2.
    • Enhanced ACE and ACE2 activity, activating the ACE2-Ang1-7-Mas axis.
    • Inhibited ACE expression and protein, alleviating Ang II-induced myocardial damage.

    Conclusions:

    • β-CM7 activates the protective ACE2-Angiotensin-(1-7)-Mas axis in the RAS.
    • β-CM7 mitigates myocardial damage in diabetic rats, potentially via the ACE/ACE2 pathway.

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