Effects of phytosterol ester on aortic aging and expression of related genes in rats
10.3969/j.issn.1000-4718.2017.08.004
- VernacularTitle:植物甾醇酯对大鼠主动脉衰老及相关基因表达的影响
- Author:
Chengcheng DING
;
Wenfang LI
;
Jin ZHOU
;
Ke RAN
;
Xiaoqing WU
;
Shuang RONG
- Keywords:
Phytosterol ester;
Aortic aging;
Silent information regulator 1;
Peroxisome proliferator-activated receptor γ
- From:
Chinese Journal of Pathophysiology
2017;33(8):1365-1370
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the protective effect of phytosterol ester (PSE) on aortic aging in rats.ME-THODS: The female SD rats (12 months old, n=42) were randomly divided into control group, model group and PSE group.During the experiment, the rats in control group, model group and PSE group were treated with basic feed, high-fat diet (HFD) and HFD with 2% PSE (W/W) for 6 months, respectively.The morphological changes of the aorta were observed by HE staining and Masson staining, and the absolute area of smooth muscle cells and collagen fiber in the vascular wall were measured by image analysis.The levels of advanced glycosylation end products (AGEs), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) in the plasma were detected.The expression of silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor γ (PPARγ) at mRNA and protein levels in the vascular tissue was determined by real time PCR and Western blot, respectively.RESULTS: PSE significantly lowered plasma TC and LDL-C, and increased plasma HDL-C level (P<0.05), but had no effect on plasma TG level.PSE significantly attenuated the thickening of intima and media of aging aortic, and decreased the migration of vascular smooth muscle cells (VSMC) and the amount of VSMC and collagen fiber in the aorta (P<0.05).PSE significantly reduced the contents of AGEs and MDA (P<0.05), but had no effect on the activity of SOD and CAT in the plasma.PSE also down-regulated the expression of PPARγ and up-regulated the expression of SIRT1 (P<0.05).CONCLUSION: PSE is able to attenuate the senescence process in the aorta by reducing the production of reactive oxygen species in plasma, and activating SIRT1, or inhibiting the expression of PPARγ in vascular tissues.
