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Carvacrol Attenuates Diabetic Cardiomyopathy by Modulating the PI3K/AKT/GLUT4 Pathway in Diabetic Mice
Ning Hou1,2, Yunpei Mai1,2,3, Xiaoxia Qiu1,2
1Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Abstract:
Background: Diabetic cardiomyopathy (DCM), a common complication of diabetes mellitus, eventually leads to heart failure. Carvacrol is a food additive with diverse bioactivities. We aimed to study the protective effects and mechanisms of carvacrol in DCM. Methods: We used a streptozotocin-induced and db/db mouse model of types 1 and 2 diabetes mellitus (T1DM and T2DM), respectively. Both study groups received daily intraperitoneal injections of carvacrol for 6 weeks. Cardiac remodeling was evaluated by histological analysis. We determined gene expression of cardiac remodeling markers (Nppa and Myh7) by quantitative real-time PCR and cardiac function by echocardiography. Changes of PI3K/AKT signaling were determined with Western blotting. GLUT4 translocation was evaluated by Western blotting and immunofluorescence staining. Results: Compared with control mice, both T1DM and T2DM mice showed cardiac remodeling and left ventricular dysfunction. Carvacrol significantly reduced blood glucose levels and suppressed cardiac remodeling in mice with T1DM and T2DM. At the end of the treatment period, both T1DM and T2DM mice showed lesser cardiac hypertrophy, Nppa and Myh7 mRNA expressions, and cardiac fibrosis, compared to mice administered only the vehicle. Moreover, carvacrol significantly restored PI3K/AKT signaling, which was impaired in mice with T1DM and T2DM. Carvacrol increased levels of phosphorylated PI3K, PDK1, AKT, and AS160 and inhibited PTEN phosphorylation in mice with T1DM and T2DM. Carvacrol treatment promoted GLUT4 membrane translocation in mice with T1DM and T2DM. Metformin was used as the positive drug control in T2DM mice, and carvacrol showed comparable effects to that of metformin on cardiac remodeling and modulation of signaling pathways. Conclusion: Carvacrol protected against DCM in mice with T1DM and T2DM by restoring PI3K/AKT signaling-mediated GLUT4 membrane translocation and is a potential treatment of DCM.
Insights
Carvacrol, a food additive, protects against diabetic cardiomyopathy (DCM) in mouse models of type 1 and type 2 diabetes mellitus (T1DM and T2DM). It improves cardiac function and reduces remodeling by enhancing PI3K/AKT signaling and GLUT4 translocation.
Area of Science:
- Cardiovascular Research
- Metabolic Disorders
- Pharmacology
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of diabetes mellitus, often progressing to heart failure.
- Carvacrol, a natural compound found in food, possesses various biological activities.
- Understanding carvacrol's protective mechanisms in DCM is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To investigate the protective effects of carvacrol on diabetic cardiomyopathy (DCM) in mouse models.
- To elucidate the underlying molecular mechanisms of carvacrol's action in DCM.
Main Methods:
- Utilized streptozotocin-induced (type 1 diabetes mellitus, T1DM) and db/db (type 2 diabetes mellitus, T2DM) mouse models.
- Administered carvacrol intraperitoneally for 6 weeks, assessing cardiac remodeling, cardiac function (echocardiography), gene expression (Nppa, Myh7), PI3K/AKT signaling pathways, and GLUT4 translocation.
Main Results:
- Carvacrol treatment significantly reduced blood glucose levels and ameliorated cardiac remodeling and left ventricular dysfunction in both T1DM and T2DM mice.
- Carvacrol suppressed cardiac hypertrophy, Nppa and Myh7 mRNA expression, and cardiac fibrosis.
- Carvacrol restored impaired PI3K/AKT signaling by increasing phosphorylation of key proteins and promoted GLUT4 membrane translocation, comparable to metformin in T2DM models.
Conclusions:
- Carvacrol demonstrates significant protective effects against DCM in both T1DM and T2DM mouse models.
- The mechanism involves the restoration of PI3K/AKT signaling pathway-mediated GLUT4 membrane translocation.
- Carvacrol represents a promising therapeutic agent for the treatment of diabetic cardiomyopathy.
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