Expression levels of SIRT1 and oxidative stress injury markers in a mouse model of deep venous thrombosis

doi:10.3969/j.issn.2095-4344.0301

Abstract

Abstract:

BACKGROUND: Silent information regulator1 (SIRT1) has been shown to inhibit oxidative stress and reduce arterial thrombosis. But changes in SIRT1 expression and oxidative stress in venous thrombosis remain unclear.
OBJECTIVE: To further analyze the correlation of SIRT1 and oxidative stress in deep venous thrombosis.
METHODS: Ninety C57 mice were randomized into three groups based on body mass: control, sham operation and model groups (n=30 per group). The mouse model of deep venous thrombosis was created by inferior vena cava stenosis, and the inferior vena cava tissues were gained at 24 hours after modeling. The thrombosis was observed by hematoxylin-eosin staining; the content of reactive oxygen species was assayed by membrane permeable fluorescent probe DCFH-DA and flow cytometry; contents of superoxide dismutase and malondialdehyde were tested; SIRT1 protein expression was detected by western blot assay.
RESULTS AND CONCLUSION: Compared with the control and sham operation groups, in the modeling group, the contents of reactive oxygen species and malondialdehyde were significantly increased, and the level of superoxide dismutase was significantly decreased (P < 0.05). The expression level of SIRT1 in the modeling group was significantly lower than that in the control and modeling groups (P < 0.05). In summary, oxidative stress plays a significant part in the germination and growth of deep venous thrombosis, and the activity of SITR1 is inhibited during deep venous thrombosis formation.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Venous Thrombosis, Models, Animal, Oxidative Stress, Superoxide Dismutase, Malondialdehyde, Tissue Engineering

CLC Number:

R318

Zhao Chong-yu, Wang Bing, Lou Zhen-kai, Li Xing-guo, He Wei, Zhao Xue-ling. Expression levels of SIRT1 and oxidative stress injury markers in a mouse model of deep venous thrombosis[J]. Chinese Journal of Tissue Engineering Research, 2018, 22(28): 4518-4524.

Figures/Tables 1

References

[1] 中华医学会骨科学分会.中国骨科大手术静脉血栓栓塞症预防指南[J].中华骨杂志，2016,36(2):65- 71

[2] Beckman MG, Hooper WC, Critchley SE,et al.Venous thromboembolism: a public health concern.Am J Prev Med, 2010;38(4):495-501.

[3] Ashrani AA,Heit JA.Incidence and cost burden of post-thrombotic syndrome.J Thromb Thrombolysis.2009; 28(4):465-476.

[4] Hill J,Treasure T,Guideline Development Group.Reducing the risk of venous (deep vein thrombosis and pulmonary embolism)in patients admitted to hospital:summary of the NICE guideline.Hear.2010;96(11):879-882.

[5] Laporte S,Mismetti P,Décousus H,et al.Clinical predictors for fatal pulmonary embolism in 15,520 patients with venous thromboembolism:findings from the Registro Informatizado de la Enfermedad TromboEmbolica venosa(RIETE) Registry. Circulation. 2008;117(13):1711-171 6.

[6] Ho KM,Burrell M,Rao S,et al.Incidence and risk factors for fatal pulmonary embolism after major trauma:a nested cohort study.Br J Anaesth.2010;105(5): 596-602.

[7] López JA,Chen J.Pathophysiology of venous thrombosis.Thromb Res.2009;123(Suppl 4):S30-34.

[8] Wakefield TW,Myers DD,Henke PK.mechanisms of venous thrombosis and resolution.Arterioscler Thromb Vasc Biol. 2008;28(3):387-391.

[9] Guo H,Chen Y,Liao L,et al.Resveratrol protects HUVECs from oxidized-LDL induced oxidative damage by autophagy upregulation via the AMPK/SIRT1 pathway.Cardiovasc Drugs ther.2016; 27(3):189-198.

[10] Hu YX,Cui H,Fan L,et al.Resveratrol attenuates left ventricular remodeling in old rats with COPD induced by cigarette smoke exposure and LPS instillation.Can J Physiol pharmacol. 2013;91(12):1044-1054.

[11] Li Y,Wang K,Feng Y,et al.Novel role of silent information regulator 1 in acute endothelial cell oxidative stress injury.Biochim Biophys Acta.2014;1842(11):2246-2256.

[12] Brandl A,Meyer M,Bechmann V,et al.Oxidative stress induces senescence in human mesenchymal stem cells.Exp Cell Res. 2011;317(11):1541-1547.

[13] 李文,胡继红,李兴国,等.KLF6通过上调TGF-β1诱导静脉内皮细胞endoglin,P-selectin表达,引发血小板黏附、聚集,促进TDVT形成的实验研究[J].中国矫形外科杂志,2011,19(16): 1365-1368.

[14] 李兴国,郑宏宇,李文,等.氧化应激和Rac1/2对静脉壁的影响及在创伤性深静脉血栓形成中的作用[J].中国组织工程研究, 2012,16(11): 2033-2038.

[15] 李兴国,郑宏宇,李文,等.深静脉血栓形成模型大鼠股静脉内皮组织中核转录因子kappa B1和组织因子的表达[J].中国组织工程研究, 2012,16(7):1245-1250.

[16] Diaz JA,Obi AT,Myers DD Jr,et al.Critical review of mouse s of venous thrombosis. Arterioscler Thromb Vasc Biol.2012;32(3): 556-562.

[17] 娄振凯,彭志,周如丹,等.P选择素、P选择素糖蛋白配体1在大鼠深静脉血栓模型中的表达变化[J].中国急救医学,2016,36(2): 142-146.

[18] Yao H and Rahman I.Perspectives on translational and therapeutic aspects of SIRT1 in inflammaging and senescence.Biochem Pharmacol.2012;84(10):1332-1339.

[19] Stavrou EX,Fang C,Merkulova A,et al.Reduced thrombosis in Klkb1-/- mice is mediated by increased Mas receptor, prostacyclin, Sirt1,and KLF4 and decreased tissue factor. Blood.2015;125(4):710-719.

[20] Vassallo PF,Simoncini S,Ligi I,et al.Accelerated senescence of cord blood endothelial progenitor cells in premature neonates is driven by SIRT1 decreased expression.Blood. 2014;123(13):2116-2126.

[21] Kao CL , Chen LK , Chang YL ,et al.Resveratrol protects human endothelium from H(2)0(2) -induced oxidative stress and senescence via SirT1 activation.Atheroscler Thromb. 2010;17(9):970-979.

[22] 张敏,朱颖,胡波,等.α-actinin-4与多柔比星肾病大鼠氧化应激状态的关系[J].实用儿科临床杂志,2009,24(5):358-360.

[23] 廖永晖,汤雨,千年松,等.氧化应激与细胞凋亡[J].新乡医学院学报,2011,28(1):110-113.

[24] Choy JC,Granville DJ,Hunt DW,et al.Endothelial cell apoptosis:biochemical characteristics and potential implications for atherosclerosis.J Mol Cell Cardiol.2001；33(9):1673-1690.

[25] Li AE,Ito H,Rovira II,et al.A role for reactive oxygen species in endothelial cell anoikis. Circ Res,1999,85(4):304-310.

[26] Turrens JF.Mitochondrial formation of reactive oxygen species. Physiol.2003;552(Pt 2):335-344.

[27] Zeng M,Wei X,Wu Z,et al.Reactive oxygen species contribute to simulated ischemia/reperfusio -n -induced autophagic cell death in human umbilical vein ehdothelial cells.Med Sci Monit.2014;19(20): 1017-1023.

[28] Gül N,Bögels M,Grewal S,et al.Surgery-induced reactive oxygen species enhance colon carcinoma cell binding by disrupting the liver endothelial cell lining.Gut.2011;60(8):1 076-1086.

[29] 娄振凯,李兴国,张福厚,等. PI3-K/Akt和MAPKs信号通路在氧化应激诱导人脐静脉内皮细胞凋亡中的作用[J].中国急救医学, 2016,36(1):78-82.