艾塞那肽对ApoE-/-小鼠动脉粥样硬化血清抵抗素的影响

Abstract
Figure/Table
References (25)
Related Citation (15)

Download: PDF (564 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of Exenatide on serum resistin in atherosclerosis of apolipoprotein E knockout (ApoE-/-) mice. Methods Thirty six-week-old ApoE-/- male mice fed with high fat were randomly divided into model group (n = 15) and exenatide group (n = 15). The exenatide group was given Exenatide 1.0 nmol/(kg·d), subperitoneal injection twice a day. Male C57BL/6J mice fed with high fat were selected as control group (n = 15). After 12 weeks, the serum was collected and the levels of total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol and triglyceride were measured by automatic biochemical analyzer. The contents of resistin, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay. The aortic root was pathologically sliced and stained with hematoxylin-eosin (HE), and the corrected patch area was measured. Results The levels of total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and triglyceride in the model group were significantly higher than those in the control group(P < 0.01). There was no significant difference in total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and triglyceride between the exenatide group and the model group (P > 0.05); the levels of resistin, TNF-α and IL-6 in the model group were significantly higher than those in the control group (P < 0.01), while the contents of resistin, TNF-α and IL-6 in the exenatide group were significantly lower than those in the model group (P < 0.01). The area of corrected atherosclerosis plaque in the exenatide group was significantly smaller than that in the model group (P < 0.05). Conclusion Exenatide can effectively reduce the level of serum resistin in atherosclerotic mice, thereby inhibiting inflammatory response and atherosclerotic plaque progression, which may be one of the mechanisms of glucagon-like peptide-1 receptor agonists in anti-atherosclerosis.

Key words： Exenatide Atherosclerosis Resistin；Glucagon-like peptide-1

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	DEND Guoxiong WEI Jinru CHEN Meixiang

Cite this article:

DEND Guoxiong WEI Jinru CHEN Meixiang. Effect of Exenatide on serum resistin in ApoE-/- mice with atherosclerosis[J]. 中国医药导报, 2019, 16(13): 4-7,11.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I13/4

[1] Steppan CM，Bailey ST，Bhat S，et al. The hormone resistin links obesity to diabetes [J]. Nature，2001，409（6818）：307-312.
[2] Reilly MP，Lehrke M，Wolfe ML，et al. Resistin is an inflammatory marker of atherosclerosis in humans [J]. Circulation，2005，111（7）：932-939.
[3] Efstathiou SP，Tsiakou AG，Tsioulos DI，et al. Prognostic significance of plasma resistin levels in patients with atherothrombotic ischemic stroke [J]. Clin Chim Acta，2007， 378（1/2）：78-85.
[4] Cheng JM，Akkerhuis KM，Battes LC，et al. Biomarkers of heart failure with normal ejection fraction：a systematic review [J]. Eur J Heart Fail，2013，15（12）：1350-1362.
[5] Falcao-Pires I，Castro-Chaves P，Miranda-Silvad，et al. Physiological，pathological and potential therapeutic roles of adipokines [J]. Drug Discov Today，2012，17（15/16）：880-889.
[6] Gencer B，Auer R，Derekeneire N，et al. Association between resistin levels and cardiovascular disease events in older adults：the health，aging and body composition study [J]. Atherosclerosis，2016，245：181-186.
[7] Park HK，Kwak MK，Kim HJ，et al. Linking resistin，inflammation，and cardiometabolic diseases [J]. Korean J Intern Med，2017，32（2）：239.
[8] 王立坤，杨占清，张军，等.2型糖尿病患者血清抵抗素、瘦素、脂联素水平与微血管病变的关系 [J].重庆医学，2017， 46（16）：2200-2203.
[9] 李伟芳，王鹏，李华，等.抵抗素水平和老年2型糖尿病患者心血管病变的关系[J].中国老年学杂志，2017，37（19）：4798-800.
[10] Koska J，Sands M，Burciu C，et al. Exenatide Protects Against Glucose- and Lipid-Induced Endothelial Dysfunction：Evidence for Direct Vasodilation Effect of GLP-1 Receptor Agonists in Humans [J]. Diabetes，2015，64（7）：2624-2635.
[11] Viola J，Soehnlein O. Atherosclerosis - A matter of unresolved inflammation [J]. Semin Immunol，2015，27（3）：184-193.
[12] Fredman G，Tabas I. Boosting Inflammation Resolution in Atherosclerosis：The Next Frontier for Therapy [J]. Am J Pathol，2017，187（6）：1211-1221.
[13] Ohira H，Tsutsui W，Fujioka Y. Are Short Chain Fatty Acids in Gut Microbiota Defensive Players for Inflammation and Atherosclerosis? [J]. J Atheroscler Thromb，2017，24（7）：660-672.
[14] Wu MY，Li CJ，Hou MF，et al. New Insights into the Role of Inflammation in the Pathogenesis of Atherosclerosis [J]. Int J Mol Sci，2017，18（10）：E2034.
[15] Ridker PM，Everett BM，Thuren T，et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease [J]. N Engl J Med，2017，377（12）：1119-1131.
[16] Groh L，Keating ST，Joosten LAB，et al. Monocyte and macrophage immunometabolism in atherosclerosis [J]. Semin Immunopathol，2018，40（2）：203-214.
[17] Silswal N，Singh Ak，Aruna B，et al. Human resistin stimulates the pro-inflammatory cytokines TNF-α and IL-12 in macrophages by NF-κB-dependent pathway [J]. Biochem Biophys Res Commun，2005，334（4）：1092-1101.
[18] Manduteanu I，Pirvulescu M，Gan AM，et al. Similar effects of resistin and high glucose on P-selectin and fractalkine expression and monocyte adhesion in human endothelial cells [J]. Biochem Biophys Res Commun，2010， 391（3）：1443-1448.
[19] Burnett MS，Lee CW，Kinnaird TD，et al. The potential role of resistin in atherogenesis [J]. Atherosclerosis，2005，182（2）：241-248.
[20] Jamaluddin MS，Yan S，Lu J，et al. Resistin increases monolayer permeability of human coronary artery endothelial cells [J]. PLoS One，2013，8（12）：e84 576.
[21] Chen C，Jiang J，Lu JM，et al. Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells [J]. Am J Physiol Heart Circ Physiol，2010，299（1）：H193-H201.
[22] Favaro E，Granata R，Miceli I，et al. The ghrelin gene products and exendin-4 promote survival of human pancreatic islet endothelial cells in hyperglycaemic conditions，through phosphoinositide 3-kinase/Akt，extracellular signal-related kinase （ERK） 1/2 and cAMP/protein kinase A （PKA） signalling pathways [J]. Diabetologia，2012， 55（4）：1058-1070.
[23] Schernthaner G. Diabetes and Cardiovascular Disease：Is intensive glucose control beneficial or deadly? Lessons from ACCORD，ADVANCE，VADT，UKPDS，PROactive，and NICE-SUGAR [J]. Wien Med Wochenschr，2010， 160（1/2）：8-19.
[24] Laake JP，Stahl D，Amiel SA，et al. The association between depressive symptoms and systemic inflammation in people with type 2 diabetes：findings from the South London Diabetes Study [J]. Diabetes Care，2014，37（8）：2186-2192.
[25] Mohamed HG，Idris SB，Ahmed MF，et al. Influence of type 2 diabetes on local production of inflammatory molecules in adults with and without chronic periodontitis：a cross-sectional study [J]. BMC Oral Health，2015， 15（1）：86.