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Protective Role of Taraxasterol against Cardiovascular Aging and Aging-Induced Desensitization of Insulin Signaling
Guangzhi Li1, Dongmei Zhang2, Shizhen Wang1
1Department of Basic Medical, Jiangsu College of Nursing, 223005 HuaiAn, Jiangsu, China.
Insights
Taraxasterol effectively reduces cardiomyocyte aging and fibrosis by regulating oxidative stress and inflammation. This compound also improves insulin signaling sensitivity, offering potential as a treatment for age-related cardiovascular diseases.
Area of Science:
- Cardiovascular research
- Aging biology
- Pharmacology
Background:
- Cardiovascular disease (CVD) is a leading global cause of death, exacerbated by population aging.
- Aging impairs cardiomyocyte function, leading to structural heart changes and CVD.
- Myocardial aging is a key factor in heart diseases, making cardiac aging mitigation crucial.
Purpose of the Study:
- To evaluate the potential of taraxasterol in mitigating myocardial aging.
- To investigate taraxasterol's effects on cardiomyocyte senescence and insulin signaling.
Main Methods:
- Analyzed taraxasterol's effect on cardiomyocyte aging in vivo and in vitro using a D-galactose mouse model.
- Assessed aging-induced desensitization of insulin signaling.
- Evaluated cardiomyocyte senescence via Sa-β-gal staining and senescence markers (p16, p21).
Main Results:
- Taraxasterol significantly alleviated cardiomyocyte senescence in vitro.
- The compound reduced oxidative stress and inflammatory processes contributing to senescence.
- Taraxasterol improved insulin signaling sensitivity and reduced cardiovascular aging and fibrosis in vivo.
Conclusions:
- Taraxasterol demonstrates potential in reducing cardiac aging and fibrosis.
- The compound enhances insulin signaling sensitivity, suggesting therapeutic applications.
- Taraxasterol may serve as an effective drug or health food additive for cardiac aging and fibrosis.
Background:
Cardiovascular disease (CVD) has become one of the leading causes of death and disability worldwide, and its incidence continues to increase because of an aging population. Studies have shown that the function of cardiomyocytes decreases during aging, leading to changes in the functional and structural integrity of the heart, ultimately resulting in CVD. The decrease in the number of functional cardiomyocytes has a negative impact on cardiac function; thus, myocardial aging is one of the main factors that causes heart-related diseases (such as CVD). Therefore, alleviating cardiac aging is one of the main ways of treating aging-related cardiac diseases. In this study, we evaluated the potential effect of taraxasterol on myocardial aging.
Methods:
The effect of taraxasterol on the aging of cardiomyocytes was analyzed in vivo and in vitro using a D-galactose treatment mouse model of cardiomyocyte senescence. Furthermore, the effect of taraxasterol on aging-induced desensitization of insulin signaling was also evaluated.
Results:
The experimental results indicated that taraxasterol could reduce cardiomyocyte senescence, which was evaluated using Sa-β-gal staining and senescence-related marker molecules (e.g., p16 and p21). We found that taraxasterol could significantly alleviate cardiomyocyte senescence in the in vitro cell model. Furthermore, we found that taraxasterol had the potential to alleviate cardiomyocyte senescence via the regulation of oxidative stress and inflammatory processes. Additionally, taraxasterol could relieve the desensitization of insulin signaling caused by aging. Finally, we showed that cardiovascular aging and fibrosis were alleviated by taraxasterol treatment in vivo.
Conclusions:
Taken together, this work illustrated that taraxasterol could reduce cardiac aging and fibrosis and enhance insulin signaling sensitivity, indicating that taraxasterol may be an effective drug or health food additive for treating cardiac aging and fibrosis.
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