Coenzyme Q10 protects against hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient mice.

Xiaoqing Zhang, Hongyang Liu, Yuhua Hao, Lulu Xu, Tiemei Zhang, Yingshu Liu, Lipeng Guo, Liyue Zhu, Zuowei Pei
Author Information
  1. Xiaoqing Zhang: Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China.
  2. Hongyang Liu: Department of Heart Intensive Care Unit, the First Affiliated Hospital of Dalian Medical University, No.193 Lianhe Road, Dalian, China.
  3. Yuhua Hao: Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China.
  4. Lulu Xu: Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China.
  5. Tiemei Zhang: Department of Infection, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China.
  6. Yingshu Liu: Department of Endocrinology, Dalian Municipal Central Hospital, 42 Xuegong Road, Dalian, China.
  7. Lipeng Guo: Department of Cardiology, Dalian Third People' Hospital Affiliated to Dalian Medical University, No.40 Qianshan Road, Dalian, China.
  8. Liyue Zhu: Rehabilitation Center, Zhejiang Hospital, 12 Lingyin Road, Hangzhou, Zhejiang, China.
  9. Zuowei Pei: Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University, No. 6 Jiefang Street, Dalian, China. pzw_dl@163.com. ORCID

Abstract

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 ApoEHD + 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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Grants

  1. 2015C33121/The social development project of public welfare technology

MeSH Term

Animals
Aorta
Apolipoproteins E
Atherosclerosis
Cardiovascular Diseases
Diet, High-Fat
Disease Models, Animal
Gene Expression Regulation
Heart Injuries
Hyperlipidemias
Interleukin-6
Mice
Protective Agents
Risk Factors
Triglycerides
Tumor Necrosis Factor-alpha
Ubiquinone

Chemicals

Apolipoproteins E
Interleukin-6
Protective Agents
Triglycerides
Tumor Necrosis Factor-alpha
Ubiquinone
coenzyme Q10

Word Cloud

Created with Highcharts 10.0.0miceApoECoQ10cardiacdamagegroupfedC57BL/6dietHDCoenzymeQ10protectsapolipoproteinE-deficientnormal+high-fatHD + CoQ10sampleshearttissuesBACKGROUND:Hyperlipidemiawell-establishedriskfactorcanleadcardiovasculardiseasesManystudiesshownvivoaimstudyinvestigatepossibleprotectiveeffectsMETHODS:Eight-week-oldmalerandomlydividedfourgroups:C57BL/6 + CoQ10groupsdifferentdiets16 weeksBloodobtainedinferiorvenacavacollectedserumtubesstored- 80 °CusedCoronalsectionsfixed10%formalinembeddedparaffinhistologicalevaluationremaindersnap-frozenliquidnitrogenmRNAimmunohistochemicalanalysisRESULTS:metabolicparameterstotalcholesterolTClow-densitylipoprotein-cholesterolLDL-ctriglyceridesTGlevelslowerApoEHD + CoQ10significantpathophysiologicalchangesH&EPASMassonCD68stainingcomparedreducedHD-inducedtissueviaautophagyp62LC3evidencedimmunoblottingimmunohistochemistryRT-qPCRalsoinhibitedinflammationIL-6TNF-αgeneexpressionCONCLUSIONS:resultsindicatepotentialtherapeutictargetcausedhyperlipidemiahyperlipidemia-induced

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