期刊
EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 18, 期 4, 页码 2451-2458出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2019.7851
关键词
atherosclerosis; autophagy; inflammation; quercetin
资金
- National Natural Science Foundation of China [81873348]
- Shanghai Nature Science Fund [16ZR1433900]
- Shanghai Health and Family Planning Commission Fund [201640217]
The present study examined the involvement of autophagy as a mechanism in the protective effect of quercetin (QUE) on atherosclerosis (AS) in ApoE(-/-) mice. An AS model was established by feeding ApoE(-/-) mice a high-fat diet (HFD). Mice were divided into four experimental groups: The model, QUE, 3-methyladenine (3-MA) and QUE + 3-MA groups. Additionally, age-matched wild-type C57BL/6 mice were used as a Control group. Autophagosomes in the aorta were examined using a transmission electron microscope. Aorta pathology, serum lipid accumulation and collagen deposition were determined by hematoxylin and eosin, Oil Red O and Masson staining, respectively. The levels of cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-18 (IL-18) were measured using ELISA assays. Protein levels of mTOR, microtubule associated protein 1 light chain 3a (LC3), P53 and cyclin dependent kinase inhibitor 1A (P21) in the aorta were analyzed using western blotting. ApoE(-/-) mice which were fed HFD exhibited substantial AS pathology, no autophagosomes, higher levels of TNF-alpha, IL-1 beta, IL-18 and mTOR and lower ratios of LC3 II/I. All these alterations were ameliorated and aggravated by QUE and 3-MA treatment, respectively. The inhibition of AS by QUE may be associated with the enhancement of autophagy and upregulation of P21 and P53 expression.
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