Effect of atorvastatin on ventricular remodeling in spontaneous hypertension rats
Shengxing Tang
Abstract
Shengxing Tang
Abstract
AIM: To explore the effect of atorvastatin on cardiac remodeling in spontaneous hypertension rats(SHR).METHODS: Twelve spontaneous hypertension rats were divided randomly into two groups: group of atorvastatin(atorvastatin 50 mg·kg~(-1)·d~(-1)) and group of SHR(0.5% mucilage of arabic gum,10 mL·kg~(-1)·d~(-1)).Additionally,six male Wistar-Kyoto rats(0.5% mucilage of arabic gum,10 mL·kg~(-1)·d~(-1)) were selected as control group.Systolic blood pressure was assessed with the tail-cuff method.After six weeks,entire heart,and left ventricle were weighed.The left ventricular weight index was calculated and myocardial hydroxyproline and collagen protein concentration were measured.The serum high sensitivity CRP(hs-CRP) was measured by nephelometry.The localization of vascular cell adhesion molecule(VCAM) in myocardium was investigated by immunohistochemistry assays.The level of NF-κB mRNA expression was detected with in situ hybridization.Ultrastructure in cardiac muscle was also observed under transmission electron microscope.RESULTS: The expression of myocardial VCAM and NF-κB in SHR group was stronger than that in WHY group.Compared with SHR group,entire heart weight,left ventricular weight,left ventricular weight index,serum hs-CRP,myocardial hydroxyproline and collagen protein concentration was decreased,the expression of myocardial VCAM and NF-κB in SHR group was weaker than that in atorvastatin treatment group.The myocardial pathological change such as incomplete karyotheca in cardiac muscle cells,no clear of transverse striation and the mess in myofibril alignment,and hyperplasy in interstitial collagen fibre were observed in SHR group and these changes were improved in atorvastatin treatment group.CONCLUSION: The cardiac remodeling in SHR is improved by atorvastatin.The molecular mechanism may be related to its down-regulating the expression of VCAM protein and NF-κB and inhibiting myocardial chronic inflammation.
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AIM: To explore the effect of atorvastatin on cardiac remodeling in spontaneous hypertension rats(SHR).METHODS: Twelve spontaneous hypertension rats were divided randomly into two groups: group of atorvastatin(atorvastatin 50 mg·kg~(-1)·d~(-1)) and group of SHR(0.5% mucilage of arabic gum,10 mL·kg~(-1)·d~(-1)).Additionally,six male Wistar-Kyoto rats(0.5% mucilage of arabic gum,10 mL·kg~(-1)·d~(-1)) were selected as control group.Systolic blood pressure was assessed with the tail-cuff method.After six weeks,entire heart,and left ventricle were weighed.The left ventricular weight index was calculated and myocardial hydroxyproline and collagen protein concentration were measured.The serum high sensitivity CRP(hs-CRP) was measured by nephelometry.The localization of vascular cell adhesion molecule(VCAM) in myocardium was investigated by immunohistochemistry assays.The level of NF-κB mRNA expression was detected with in situ hybridization.Ultrastructure in cardiac muscle was also observed under transmission electron microscope.RESULTS: The expression of myocardial VCAM and NF-κB in SHR group was stronger than that in WHY group.Compared with SHR group,entire heart weight,left ventricular weight,left ventricular weight index,serum hs-CRP,myocardial hydroxyproline and collagen protein concentration was decreased,the expression of myocardial VCAM and NF-κB in SHR group was weaker than that in atorvastatin treatment group.The myocardial pathological change such as incomplete karyotheca in cardiac muscle cells,no clear of transverse striation and the mess in myofibril alignment,and hyperplasy in interstitial collagen fibre were observed in SHR group and these changes were improved in atorvastatin treatment group.CONCLUSION: The cardiac remodeling in SHR is improved by atorvastatin.The molecular mechanism may be related to its down-regulating the expression of VCAM protein and NF-κB and inhibiting myocardial chronic inflammation.
Key concepts: Atorvastatin, Hydroxyproline, Internal medicine, Ventricle, Medicine, Myocardial infarction, Ventricular remodeling, Endocrinology