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EFFECTS OF ATORVASTATIN ON METHYLATION AND MRNA EXPRESSION OF BCL-2 IN HYPERLIPIDAEMIA WISTAR RATS
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Objectives
To investigate effects of atorvastatin on methylation status of bcl-2 gene promoter and mRNA expression of bcl-2 in aortic tissue of hyperlipidaemia Wistar rats.
Methods
66 Wistar rats were equally randomised into three groups: control group, hyperlipidaemia group and hyperlipoidaemia rat with atorvastatin group. The rats in control group were fed a normal chaw, and the other groups were fed a chaw formula as designed for 12 weeks. From the 12th week gavage experiment, after 4 weeks of heart blood was then drawn for detection of serum cholesterol, triglyceride, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol; aortic nucleoprotein was extracted for detection of DNA methyltransferase activity. The methylation specific polymerase chain reaction (MSP) method was used to detect bcl-2 gene methylation in aortic tissue of control group, hyperlipidemia group and hyperlipoidemia rat with atorvastatin group. The expression of bcl-2 mRNA in aortic tissue of control group and hyperlipidaemia group Wistar rats was detected by real-time quantitative polymerase chain reaction.
Results
A high-fat diet for 12 weeks is sufficient to induce hyperlipidaemia; Atorvastatin supplementation to the rats fed the high-fat diet prevented an elevation total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-C) and increase high density lipoprotein-cholesterol (HDL-C) levels in the serum (p<0.05) and morphological changes in the thoracic aorta. Compared with the control group, hyperlipidaemia group significantly increased DNA methyltransferase activity and methylation status of bcl-2 gene promoter (p<0.05), the expression of bcl-2 mRNA was decreased in hyperlipidaemia groups (p<0.05). Compared with the hyperlipidaemia group, atorvastatin group significantly decreased DNA methyltransferase activity and methylation status of bcl-2 gene promoter (p<0.05), the expression of bcl-2 mRNA was increased in hyperlipidaemia groups (p<0.05).
Conclusions
Atorvastatin supplementation can blunt the rise in methylation status of bcl-2 gene promoter but also can increase the expression of bcl-2 mRNA in the aorta of rats with hyperlipidaemia. The study provide new ideas for prevention and delay of atherosclerosis.
Title: EFFECTS OF ATORVASTATIN ON METHYLATION AND MRNA EXPRESSION OF BCL-2 IN HYPERLIPIDAEMIA WISTAR RATS
Description:
Objectives
To investigate effects of atorvastatin on methylation status of bcl-2 gene promoter and mRNA expression of bcl-2 in aortic tissue of hyperlipidaemia Wistar rats.
Methods
66 Wistar rats were equally randomised into three groups: control group, hyperlipidaemia group and hyperlipoidaemia rat with atorvastatin group.
The rats in control group were fed a normal chaw, and the other groups were fed a chaw formula as designed for 12 weeks.
From the 12th week gavage experiment, after 4 weeks of heart blood was then drawn for detection of serum cholesterol, triglyceride, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol; aortic nucleoprotein was extracted for detection of DNA methyltransferase activity.
The methylation specific polymerase chain reaction (MSP) method was used to detect bcl-2 gene methylation in aortic tissue of control group, hyperlipidemia group and hyperlipoidemia rat with atorvastatin group.
The expression of bcl-2 mRNA in aortic tissue of control group and hyperlipidaemia group Wistar rats was detected by real-time quantitative polymerase chain reaction.
Results
A high-fat diet for 12 weeks is sufficient to induce hyperlipidaemia; Atorvastatin supplementation to the rats fed the high-fat diet prevented an elevation total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-C) and increase high density lipoprotein-cholesterol (HDL-C) levels in the serum (p<0.
05) and morphological changes in the thoracic aorta.
Compared with the control group, hyperlipidaemia group significantly increased DNA methyltransferase activity and methylation status of bcl-2 gene promoter (p<0.
05), the expression of bcl-2 mRNA was decreased in hyperlipidaemia groups (p<0.
05).
Compared with the hyperlipidaemia group, atorvastatin group significantly decreased DNA methyltransferase activity and methylation status of bcl-2 gene promoter (p<0.
05), the expression of bcl-2 mRNA was increased in hyperlipidaemia groups (p<0.
05).
Conclusions
Atorvastatin supplementation can blunt the rise in methylation status of bcl-2 gene promoter but also can increase the expression of bcl-2 mRNA in the aorta of rats with hyperlipidaemia.
The study provide new ideas for prevention and delay of atherosclerosis.
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