N for insulin resistance and beta-cell defects in the male ZuckerN for insulin resistance and

N for insulin resistance and beta-cell defects in the male Zucker
N for insulin resistance and beta-cell defects in the male Zucker diabetic fatty rat. Diabetes 1998, 47:358?64.doi:10.1186/1476-511X-11-78 Cite this article as: Botezelli et al.: Fructose-rich diet leads to reduced aerobic capacity and to liver injury in rats. Lipids in Health and Disease 2012 11:78.Submit your next manuscript to BioMed Central and take full advantage of:?Convenient online submission ?Thorough peer review ?No space constraints or color figure charges ?Immediate publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit
Sang et al. Lipids in Health and Disease 2012, 11:166 http://www.lipidworld.com/content/11/1/RESEARCHOpen AccessInhibitory effect of the combination therapy of simvastatin and pinocembrin on atherosclerosis in apoE-deficient miceHui Sang1,2, Na Yuan2, Shutong Yao1,2, Furong Li3, Jiafu Wang1,2, Yongqi Fang1,2* and Shucun Qin1*AbstractThe present study was Cyclopamine cost performed to investigate the effects of the combination therapy of pinocembrin and simvastatin on the atherosclerotic lesions development in the ApoE-/- mice. Methods: Eight-week-old male ApoE-/- mice were fed high fat diet (HFD) and treated with simvastatin (10 mg/kg per day), pinocembrin (20 mg/kg per day), or the combination therapy (simvastatin 5 mg/kg per day and pinocembrin 20 mg/kg per day) for 14 weeks. The serum lipid levels, nitric oxide (NO), endothelin (ET), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined with spectrophotometric measurement and ELISA assay. Vascular endothelial growth factor (VEGF) in serum and aortic root was detected. En face analyses of atherosclerotic lesion in whole aorta and aortic root PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/26780312 sections were performed with plaque staining using oil red O. Results: The combination treatment with simvastatin and pinocembrin resulted in significantly decreased levels of serum total cholesterol, triglycerides and low-density lipoprotein cholesterol, augmented NO levels and SOD activity, inhibited ET and VEGF expression. Immunohistochemistry of aortic valve sections revealed that the combination therapy also suppressed the expression of VEGF induced by HFD. In addition, HFD-induced arterial wall lipid disposition displayed by oil red O staining was reduced significantly in aortic root and whole aorta en face in the combination administrated mice. The effect of the combination was superior to simvastatin alone. Conclusion: The combination of simvastatin and pinocembrin synergistically inhibited atherosclerotic lesion development in ApoE-/- mice with hyperlipidemia, which is partially dependent on the protective of vascular endothelium. Keywords: Pinocembrin, Simvastatin, Combined therapy, Atherosclerotic lesion, Apolipoprotein E knockout miceBackground Atherosclerosis is the primary underlying cause of cardiovascular disease and the major cause of mortality in the western world today [1]. Atherogenic stimuli, including dyslipidemia and oxidative stress, induce vascular endothelial dysfunction which is considered as an early marker for atherosclerosis [2]. Vascular endothelial cells are not merely constituents of the vessel wall but are able to respond to physiological stress, which play* Correspondence: [email protected]; [email protected] Equal contributors 1 Institute of Atherosclerosis, Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Tai.