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虾青素对AngⅡ诱导的心脏成纤维细胞胶原蛋白合成的影响

Effects of Astaxanthin on the Collagen Expression of Cardiac Fibroblasts Induced by AngiotensinⅡ
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摘要 目的探讨虾青素对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心脏成纤维细胞(cardiac fibroblasts,CFs)胶原蛋白合成的影响。方法体外培养SD乳鼠的CFs,分为5组,分别为对照组、AngⅡ组、AngⅡ+虾青素低剂量组(20μmol/L)、AngⅡ+虾青素中剂量组(40μmol/L)、AngⅡ组+虾青素高剂量组(80μmol/L),干预24h后,采用Western blot法检测Ⅰ型胶原蛋白的含量,RT-PCR检测α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)的含量,活细胞计数试剂盒(CCK8)测定CFs增殖情况。结果 AngⅡ可以使Ⅰ型胶原蛋白和α-平滑肌肌动蛋白表达上升(P<0.05),CFs增殖增加,不同浓度的虾青素均可以抑制这种作用(P<0.05)。结论在一定的浓度范围内,虾青素可抑制心脏成纤维细胞胶原蛋白的合成,抑制心脏成纤维细胞的增殖。 Objective To investigate the effect of astaxanthin on the collagen expression in cardiac fihroblasts induced by Angloten- sin 1I (Ang I/ ). Methods We cultured cardiac fibroblasts(CFs) of neonatal Sprague- Dawley(SD) rats in vitro. The CFs were divided into five groups which were control group cultured without Ang Ⅱ or astaxanthin, Ang I1 group cultured with Ang Ⅱ and astaxanthin groups cultured with Ang Ⅱ and astaxanthin 20,40,801xmol/L, respectively. After 24 hours of cultivation, the level of collagen Ⅰ was detected by Western bloting, the expression of the α -smooth muscle aetin (ct -SMA)was detected by reverse transcription polymerase chain reaction ( RT - PCR) , and the proliferation of CFs was measured by CCK8 kit. Results The expression of collagen I and a - SMA were increased induced by Ang I1 ( P 〈 0.05 ) , and the proliferation of CFs was also enhanced by Ang 11 , but astaxanthin reversed these effects during co - treating with Ang Ⅱ (P 〈 0.05 ). Conclusion Within a range of given concentrations, astaxanthin can reduce the expression of collagen I and Ⅱ -SMA, and inhibit the proliferation of CFs, which indicate that astaxanthin can inhibit cardiac fibrosis.
出处 《医学研究杂志》 2018年第2期36-40,共5页 Journal of Medical Research
基金 国家自然科学基金资助项目(81170085)
关键词 虾青素 心脏成纤维细胞 心肌纤维化 I型胶原蛋白 Astaxanthin Cardiac fibroblast Cardiac fibrosis Collagen I
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  • 1姚钢炼,宁宁,高登峰,桂保松.氧化苦参碱在大鼠肾间质纤维化进程中的保护作用[J].西安交通大学学报(医学版),2006,27(3):254-257. 被引量:12
  • 2Lie-Venema H,van den Akker NM,Bax NA,et al.Origin,fate,and function of epicardium-derived cells(EPDCs)in normal and abnormal cardiac development[J].ScientificWorldJournal,2007,12(7):1 777-1 798.
  • 3Hajdu Z,Romeo SJ,Fleming PA,et al.Recruitment of bone marrow-derived valve interstitial cells is a normal homeostatic process[J].J Mol Cell Cardiol,2011,51(6):955-965.
  • 4Zhou B,von Gise A,Ma Q,et al.Genetic fate mapping demonstrates contribution of epicardium-derived cells to the annulus fibrosis of the mammalian heart[J].Dev Biol,2010,338(2):251-261.
  • 5Chu PY,Mariani J,Finch S,et al.Bone marrow-derived cells contribute to fibrosis in the chronically failing heart[J].Am J Pathol,2010,176(4):1 735-1 742.
  • 6Kong P,Christia P,Saxena A,et al.Lack of specificity of fibroblast-specific protein 1in cardiac remodeling and fibrosis[J].Am J Physiol Heart Circ Physiol,2013,305(9):H1 363-1 372.
  • 7Santiago JJ,Dangerfield AL,Rattan SG,et al.Cardiac fibroblast to myofibroblast differentiation in vivo and in vitro:expression of focal adhesion components in neonatal and adult rat ventricular myofibroblasts[J].Dev Dyn,2010,239(6):1 573-1584.
  • 8Xie J,Zhang Q,Zhu T,et al.Substrate stiffness-regulated matrix metalloprotein-ase output in myocardial cells and cardiac fibroblasts:implications for myocardial fibrosis[J].Acta Biomater,2014,10(6):2 463-2 472.
  • 9Li Q,Xu Y,Li X,et al.Inhibition of Rho-kinase ameliorates myocardial remodeling and fibrosis in pressure overload and myocardial infarction:role of TGF-beta1-TAK1[J].Toxicol Lett,2012,211(2):91-97.
  • 10Polyakova V,Loeffler I,Hein S,et al.Fibrosis in endstage human heart failure:severe changes in collagen metabolism and MMP/TIMP profiles[J].Int J Cardiol,2011,151(1):18-33.

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