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Published on: September 26, 2018
Coenzyme Q10 protects against hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient mice
Xiaoqing Zhang1, Hongyang Liu2, Yuhua Hao1
1Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China.
Insights
Coenzyme Q10 (CoQ10) supplementation reduced cardiac damage in mice with hyperlipidemia. This antioxidant protected against high-fat diet-induced heart issues by reducing inflammation and improving metabolic parameters.
Area of Science:
- Cardiovascular Research
- Nutritional Science
- Biochemistry
Background:
- Hyperlipidemia is a significant risk factor for cardiovascular disease and cardiac damage.
- Coenzyme Q10 (CoQ10) has demonstrated cardioprotective effects in various in vivo studies.
- Apolipoprotein E-deficient (ApoE-/-) mice are a relevant model for studying hyperlipidemia-induced cardiovascular pathology.
Purpose of the Study:
- To investigate the protective effects of Coenzyme Q10 (CoQ10) against cardiac damage in apolipoprotein E-deficient (ApoE-/-) mice fed a high-fat diet.
- To evaluate the impact of CoQ10 on metabolic parameters and cardiac tissue pathology in this model.
- To explore the molecular mechanisms, including autophagy and inflammation, underlying CoQ10's cardioprotective actions.
Main Methods:
- Eight-week-old male C57BL/6 and ApoE-/- mice were assigned to four groups: control, control + CoQ10, high-fat diet (HD), and HD + CoQ10.
- Mice were fed their respective diets for 16 weeks, followed by collection of blood and heart tissue samples.
- Histological evaluation (H&E, PAS, Masson, CD68 staining), immunoblotting, immunohistochemistry, and RT-qPCR were used to assess cardiac damage, autophagy markers (p62, LC3), and inflammatory gene expression (IL-6, TNF-α).
Main Results:
- CoQ10 supplementation significantly lowered total cholesterol, LDL-cholesterol, and triglyceride levels in ApoE-/- mice on a high-fat diet.
- Histopathological analysis revealed reduced cardiac tissue damage in ApoE-/- mice treated with CoQ10 compared to untreated controls.
- CoQ10 treatment modulated autophagy pathways and inhibited the expression of key inflammatory genes (IL-6, TNF-α) in the hyperlipidemic mouse hearts.
Conclusions:
- Coenzyme Q10 demonstrates significant cardioprotective effects in a mouse model of hyperlipidemia.
- CoQ10 mitigates cardiac damage by reducing lipid levels, inhibiting inflammation, and modulating autophagy.
- These findings suggest CoQ10 as a potential therapeutic agent for managing cardiac complications associated with hyperlipidemia.
Background:
Hyperlipidemia is a well-established risk factor for cardiac damage, which can lead to cardiovascular diseases. Many studies have shown that Coenzyme Q10(CoQ10) protects against cardiac damage in vivo. The aim of this study was to investigate the possible protective effects of CoQ10 against cardiac damage in apolipoprotein E-deficient (ApoE-/-) mice.
Methods:
Eight-week-old male C57BL/6 and ApoE-/- mice were randomly divided into four groups: C57BL/6 mice fed a normal diet (C57BL/6 group); C57BL/6 mice fed a normal diet + CoQ10 (C57BL/6 + CoQ10 group); ApoE-/- mice fed a high-fat diet (ApoE-/- HD group), and ApoE-/- mice fed a high-fat diet + CoQ10 (ApoE-/- HD + CoQ10 group). All groups were fed the different diets for 16 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes. The samples were then stored at - 80 °C until used. Coronal sections of heart tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The remainder of the heart tissues was snap-frozen in liquid nitrogen for mRNA or immunohistochemical analysis.
Results:
The metabolic parameters such as total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-c), and triglycerides (TG) levels were lower in ApoE-/-HD + CoQ10 mice than in ApoE-/- HD mice. There were significant pathophysiological changes (H&E, PAS, Masson and CD68 staining) in ApoE-/- mice in the HD group compared with those in the HD + CoQ10 group. CoQ10 reduced HD-induced cardiac tissue damage via autophagy (p62 and LC3), as evidenced by immunoblotting, immunohistochemistry, and RT-qPCR. CoQ10 also inhibited inflammation (IL-6 and TNF-α) gene expression in ApoE-/- mice.
Conclusions:
These results indicate that CoQ10 is a potential therapeutic target for cardiac damage caused by hyperlipidemia.
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