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| Impacts of atorvastatin on expression of IL-17a, LP-PLA2 in low-density lipoprotein receptor knockout mice |
1.Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical University,
Wenzhou, 325015; 2.Department of Cardiology, the Affiliated Hospital of Hangzhou Normal University, Hangzhou,
310015
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Abstract Objective: To investigate the effect of atorvastatin on expression of IL-17a, LP-PLA2 in LDLR-knockout (LDLR-/-) mice. Methods: Eighteen 8-week-old male LDLR-/- mice were raised in six cages. Twelve mice were fed with high fat diet for establishing atherosclerosis model. The other six mice were fed with normal diet which was used as the normal diet control group. After eight weeks, mice fed with high fat diet were divided into high fat diet control group (n=6) and atorvastatin group (n=6, 60 mg·kg-1·d-1 per gavage). The other six mice fed with normal diet which was used as normal diet control group and continued to feed normal diet. All mice were sacrificed after eight weeks. Automatic Biochemical Analyzer was performed to measure serum lipid levels. Hematoxylin and eosin (HE) staining was used to observe the morphology of plaque. qRT-PCR was performed to analyze the level of expression of IL-17a mRNA and LP-PLA2 mRNA. Immunohistochemistry was performed to analyze the expression of protein IL-17a. Western blot was performed to analyze the expression of protein LP-PLA2. Results: Serum cholesterol (TC) and low density lipoprotein (LDL) levels were significantly higher in high fat diet control group than that in normal diet control group (both P<0.05), while there were no significantly difference of triglyceride (TG) level between two groups (P>0.05). TC and LDL levels of Atorvastatin group compared with the high fat control group were significantly reduced (P<0.05). Also, there were no significantly difference of TG level between two groups (P>0.05). Obviously, Atherosclerosis lesion area was observed in high fat diet control group, while there was no atherosclerosis lesion observed in normal diet control group. The expression of IL-17a (both protein and mRNA) and LP-PLA2 (both protein and mRNA) in high fat diet control group was significantly up-regulated than that in the normal diet control group (all P<0.05). Compared with the high fat control group, atherosclerosis lesion area of the atorvastatin group was significantly decreased, and the expression of IL-17a (both protein and mRNA) and LP-PLA2 (both protein and mRNA) was significantly lower (all P<0.05). Conclusion: Atorvastatin can contribute to anti-atherosclerosis by inhibiting the expression of IL-17a and LP-PLA2, reducing inflammation in LDLR-/-mice fed with high fat diet.
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Received: 18 December 2014
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