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Potential Therapeutic Effect of Citronellal on Diabetic Cardiomyopathy in Experimental Rats
Jun-Xiu Lu1,2, Yue Qiu1, Li-Juan Guo3
1College of Pharmacy, Henan International Joint Laboratory of Cardiovascular Remodeling and Drug Intervention, Xinxiang Key Laboratory of Vascular Remodeling Intervention and Molecular Targeted Therapy Drug Development, Xinxiang Medical University, Xinxiang 453003, China.
Insights
Citronellal (CT) shows therapeutic potential for diabetic cardiomyopathy (DCM). This study found CT treatment improved cardiac function and reduced oxidative stress and apoptosis in diabetic rats by inhibiting NHE1 activation.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Diabetic cardiomyopathy (DCM) is a serious complication in diabetes, distinct from other heart conditions.
- Citronellal (CT), a plant-derived monoterpene, has potential therapeutic applications.
- Understanding CT's mechanism in DCM is crucial for developing new treatments.
Purpose of the Study:
- To investigate the therapeutic effects of Citronellal (CT) on diabetic cardiomyopathy (DCM).
- To elucidate the underlying mechanisms of CT's action in DCM, focusing on oxidative stress and ion transport.
Main Methods:
- Diabetic rat models were induced using a high-fat/high-carbohydrate diet and streptozotocin (STZ).
- Cardiac function was assessed using Doppler ultrasound; myocardial structure was analyzed via histopathology.
- Biochemical tests, immunofluorescence, and Western blot were used to measure oxidative stress markers (SOD, MDA) and protein levels (NHE1, Bax, Bcl-2).
Main Results:
- DCM rats exhibited cardiac dysfunction, hypertrophy, fibrosis, apoptosis, and increased oxidative stress (decreased SOD, increased MDA).
- Nontreated DCM rats showed abnormal sodium-hydrogen exchanger 1 (NHE1) activation and altered apoptosis markers (increased Bax, decreased Bcl-2).
- CT treatment (150 mg/kg/day) significantly improved cardiac function, reduced myocardial damage, inhibited oxidative stress, and normalized NHE1 activation.
Conclusions:
- Citronellal (CT) demonstrates a protective effect against diabetic cardiomyopathy (DCM) in a rat model.
- CT's mechanism involves the repression of abnormal sodium-hydrogen exchanger 1 (NHE1) activation.
- CT may serve as a potential therapeutic agent for managing DCM by mitigating oxidative stress and apoptosis.
Abstract:
Diabetic cardiomyopathy (DCM), a cardiovascular complication of patients with diabetes, is a special cardiomyopathy that is independent of coronary heart disease, hypertension, and valvular disease. Citronellal (CT) is a monoterpene compound generated by the secondary metabolism of plants. In this work, the therapeutic effect and mechanism of CT in DCM were investigated. Experimental diabetic rat models were constructed through a high-fat and high-carbohydrate diet combined with low-dosage streptozotocin (STZ) treatment. CT was intragastrically administered at the dosage of 150 mg/kg/day. The cardiac functions of the rats were evaluated via cardiac Doppler ultrasound. Changes in myocardial structure were analyzed through histopathology. Changes in the representative indices of oxidative stress, namely, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected on the basis of a biochemical test. Related protein levels were assayed via immunofluorescence and Western blot analyses. The DCM rats in the nontreatment group experienced diastolic and systolic dysfunctions, associated with myocardial hypertrophy, fibrosis, and cardiomyocyte apoptosis. Moreover, this condition was concurrent with metabolic disorders, the degradation of SOD activity in myocardial tissues, the increase in MDA content, the abnormal activation of sodium-hydrogen exchanger 1 (NHE1), and the aggravation of cell apoptosis (Bax levels were elevated, whereas Bcl-2 levels decreased). Myocardial hypertrophy, fibrosis, oxidative stress, and cell apoptosis were obviously inhibited after treatment with CT (150 mg/kg/day). The abnormal activation of NHE1 was recovered under the action of CT. Our study results showed that CT might play a protective role in the treatment of DCM by repressing the abnormal activation of NHE1.
