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植物甾醇酯对大鼠主动脉衰老及相关基因表达的影响 被引量:3

Effects of phytosterol ester on aortic aging and expression of related genes in rats
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摘要 目的:探讨植物甾醇酯延缓大鼠主动脉衰老的作用及其机制。方法:将42只12月龄雌性SD大鼠随机均分为对照组、模型组和植物甾醇酯干预组,分别喂食基础饲料、高脂饲料和高脂加2%植物甾醇酯(W/W)饲料6个月。采用HE染色法和Masson染色法对主动脉横截面石蜡切片进行染色,观察主动脉组织的病理学改变,对血管壁平滑肌细胞和胶原纤维的绝对面积进行图像分析。检测血浆脂质蛋白、晚期糖基化终末产物(AGEs)、丙二醛(MDA)的含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性。分别采用real-time PCR和Western blot的方法评估主动脉组织沉默信息调节因子1(SIRT1)和过氧化物酶体增殖物激活受体γ(PPARγ)的mRNA和蛋白表达水平。结果:与模型组相比,植物甾醇酯干预组的血浆总胆固醇和低密度脂蛋白胆固醇水平显著降低,高密度脂蛋白胆固醇的水平相反(P<0.05),甘油三酯的水平没有统计学差异;主动脉内膜和中膜的增厚以及平滑肌细胞的迁移均得到改善;主动脉平滑肌细胞和胶原纤维的含量显著下降(P<0.05);血浆AGEs的含量显著降低(P<0.05);机体的抗氧化功能有所提升,血浆MDA的含量显著减少(P<0.05),SOD和CAT活性的差异没有统计学意义;PPARγ的表达下调,SIRT1的表达上调(P<0.05)。结论:植物甾醇酯能够延缓大鼠主动脉的衰老。其机制可能与降低机体活性氧的生成有关。植物甾醇酯可能通过激活SIRT1或抑制PPARγ的表达而发挥作用。 A IM:To explore the protective effect of phytosterol ester(PSE)on aortic aging in rats.M E TH O D S:The female SD rats(12months old,n=42)were randomly divided into control group,model group and PSEgroup.During the experiment,the rats in control group,model group and PSE group were treated with basic feed,high-fatdiet(H FD)and HFD with2%PSE(W/W)for6months,respectively.The morphological changes of the aorta were observedby HE staining and Masson staining,and the absolute area of smooth muscle cells and collagen fiber in the vascularwall were measured by image analysis.The levels of advanced glycosylation end products(A G E s),malondialdehyde(M D A),superoxide dismutase(SOD)and catalase(CAT)in the plasma were detected.The expression of silent informationregulator1(SIRT1)and peroxisome proliferator-activated receptor y(PPAR^y)at mRNA and protein levels in the vasculartissue was determined by real time PCR and Western blot,respectively.R E SU L T S:PSE significantly lowered plasmaTC and LDL-C,and increased plasma HDL-C level(P<0.05),but had no effect on plasma TG level.PSE significantlyattenuated the thickening of intima and media of aging aortic,and decreased the migration of vascular smooth musclecells(VSMC)and the amount of VSMC and collagen fiber in the aorta(P<0.05).PSE significantly reduced the contentsof 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 PPAR^y and up-regulated the expression of SIRT1(P<0.05).CONCLUSION:PSE is able to attenuatethe senescence process in the aorta by reducing the production of reactive oxygen species in plasma,and activating SIRT1,or inhibiting the expression of PPARγin vascular tissues.
作者 丁程程 李文芳 周锦 冉钶 吴晓青 荣爽 DING Cheng-cheng;LI Wen-fang;ZHOU Jin;RAN Ke;WU Xiao-qing;RONG Shuang(School of Public Health, Medical College, Wuhan University of Science and Technology,Wuhan 430065 , China;Institute of Nutrition and Chronic Diseases, Wuhan University of Science and Technology, Wuhan 430065 , China)
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2017年第8期1365-1370,共6页 Chinese Journal of Pathophysiology
基金 2013年BASF国际健康研究基金项目课题(亚洲)
关键词 植物留醇酯 主动脉衰老 沉默信息调节因子1 过氧化物酶体增殖物激活受体Γ Phytosterol ester Aortic aging Silent information regulator 1 Peroxisome proliferator-activated receptorγ
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  • 1吕建敏,应华忠,徐孝平,王德军,周为民,王辉.高脂血症动物模型研究进展[J].浙江中医学院学报,2005,29(4):87-89. 被引量:46
  • 2[1]Andrew JB, Wendy J. Oxysterols and atherosclerosis[J]. Atherosclerosis, 1999,142(1):1-28.
  • 3[2]Guardiola F, Codony R, Addis PB, et al. Biological effects of oxysterols: current status[J]. Food Chem Toxicol, 1996, 34(2):193-211.
  • 4[3]Hennig B, Boissonneault GA. Cholestan-3β,5α,6β-triol decrease barrier function of cultured endothelial cell monolayers[J]. Atherosclerosis, 1987, 68(2):255-261.
  • 5[4]Biossoneault GA, Hennig B, Ouyang CM. Oxysterols, cholesterol biosynthesis and vascular endothelial cell monolayer barrier function[J]. Proc Soc Exp Biol Med, 1991, 196(4):338-343.
  • 6[5]Martin RB, Joseph JB. Apoptosis of vascular smooth muscle cells in artherosclerosis[J]. Atherosclerosis, 1998, 138(1):3-9.
  • 7[6]Armin H, Seigo I. Apoptosis-Basic mechanisms and implications for cardiovascular disease[J]. Circ Res, 1998, 82(11):1111-1129.
  • 8[7]Dimmeler SF, Haendeler JD, Galle J, et al. Oxidized low-density lipoprotein induces apoptosis of human endothelial cells by activation of CPP32-like proteases[J]. Circulation, 1997, 95(7):1760-1773.
  • 9[8]Shiba MH, Kinoshita M, Kamido H, et al. Oxidized LDL induced apoptosis in cultured human umbilical vein endothelial cells by common and unique mechanisms[J]. J Bio Chem, 1998, 273(16):9681-9687.
  • 10[9]Smith LL. Review of progress in sterol oxidations:1987-1995[J]. Lipids, 1996, 31(4):453-487.

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