Evaluation of endothelial function and estimation of the degree of apoptosis in patients with metabolic syndrome and non-alcoholic fatty liver disease
- 作者: Drapkina OM1, Deeva TA1, Ivashkin VT1
-
隶属关系:
- 期: 卷 87, 编号 5 (2015)
- 页面: 76-83
- 栏目: Editorial
- ##submission.dateSubmitted##: 10.04.2020
- ##submission.datePublished##: 15.05.2015
- URL: https://ter-arkhiv.ru/0040-3660/article/view/31758
- ID: 31758
如何引用文章
全文:
详细
Aim. To evaluate endothelial function (EF) and to estimate the level of a serum apoptosis marker (caspase-8) in patients with metabolic syndrome (MS) and in those with non-alcoholic fatty liver disease (NAFLD). Subjects and methods. The investigation enrolled 76 patients: 43 with MS (out of them, 72.1% were found to have NAFLD) and 33 without MS and NAFLD. All the patients underwent evaluation of EF by photoplethysmography; the level of caspase-8 as one of the apoptosis markers was studied in all. Results. Increased arterial stiffness was more common in a group of patients with MS. Systolic duration was higher in these patients (p<0.05). In these patients, an occlusion test revealed the significantly more marked signs of endothelial dysfunction (ED), which correlated with some cardiovascular diseases (CVD), and hepatic steatosis (p<0.05). The mean level of caspase-8 was significantly higher in the group of MS patients (p<0.05). There was a positive correlation between caspase-8 levels and hepatic and pancreatic steatosis, obesity, aortic atherosclerosis, type 2 diabetes mellitus, and gastroesophageal reflux disease (p<0.05). Conclusion. The study group of MS patients (among whom, there was a preponderance of those with NAFLD) had, firstly, higher arterial stiffness more frequently (as evidenced by photoplethysmography), secondly, longer systolic duration, which may be a risk factor for CVD; thirdly, more pronounced ED. Fourthly, according to the data of a study of caspase-8 levels, its indicator may serve as a prognostic marker for the development of CVD and NAFLD. It was, fifthly, shown that the administration of statins might reduce the degree of apoptosis.
参考
- Furchgott RF, Zawadzki JV. The obligatory role of the endothelial cells in relaxation of arterial smooth muscle by acetylcholine. Nature. 1980;288:373-376.
- Luscher TF, Barton M. Biology of the endothelium. Clin Cardiol. 1997;20(11 suppl 2):II-3-10.
- Behrendt D, Ganz P. Endothelial function: from vascular biology to clinical applications. Am J Cardiol. 2002;90:40L-48L.
- Ивашкин В.Т., Драпкина О.М. Клиническое значение оксида азота и белков теплового шока. М.: ГЭОТАР-Медиа; 2011
- Ross R. Atherosclerosis: aninflammatory disease. The New England Journal of Medicine. 1999;340:115-126.
- Schalkwijk CG, Stehouwer CD. Vascular complications in diabetes mellitus: the role of endothelial dysfunction. Clin Sci (Lond). 2005;109(2):143-159.
- Ludmer PL, Selwyn AP, Shook TL, Wayne RR, Mudge GH, Alexander RW, Ganz P. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. N Engl J Med. 1986;315:1046-1051.
- Rubbo H, Trostchansky A, Botti H, Batthyany C. Interactions of nitric oxide and peroxynitrite with low-density lipoprotein. Biol Chem. 2002;383:547-552.
- Steinberg D, Witztum JL. Is the oxidative modification hypothesis relevant to human atherosclerosis? Circulation. 2002;105:2107-2111.
- Ehara S, Ueda M, Naruko T, Haze K, Itoh A, Otsuka M, Komatsu R, Matsuo T, Itabe H, Takano T, Tsukamoto Y, Yoshiyama M, Takeuchi K, Yoshikawa J, Becker A. Elevated levels of low density lipoprotein show a positive relationship with the severity of acute coronary syndromes. Circulation. 2001;103:1955-1960.
- Ивашкин В.Т., Драпкина О.М. Оксид азота в регуляции функциональной активности физиологических систем. Российский журнал гастроэнтерологии, гепатологии и колопроктологии. 2000;4:16-21.
- Nguyen T, Brunson, DNA damage and mutation in human cells exposed to nitric oxide in vitro. Proc Natl Acad Sci USA. 1992;89(7):3030-3034.
- Endres M, Laufs U, Huang Z, Nakamura T, Huang P, Moskowitz MA, Liao JK. Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase. Proc Natl Acad Sci USA. 1998;95:8880-8885.
- d’Uscio LV, Milstien S, Richardson D, Smith L, Katusic ZS. Long-term vitamin C treatment increases vascular tetrahydrobiopterin levels and nitric oxide synthase activity. Circ Res. 2003;92:88-95.
- Драпкина О.М., Ашихмин Я.И., Ивашкин В.Т. Роль шаперонов в патогенезе сердечно-сосудистых заболеваний и кардиопротекции. Российские медицинские вести. 2008;1:56-69.
- Drapkina O., Ivashkin V., Ashikhmin Y. Specific characteristics of NO synthesis in myocardial infarction (thesis). Abstract book. 16 European Meeting on Hypertention, June 12-15. 2006:321.
- Драпкина О.М., Ивашкин В.Т. Оксид азота и инфаркт миокарда. Молекулярная медицина. 2004;1:37-42.
- Драпкина О.М., Деева Т.А., Волкова Н.П. Фиброз у пациентов с метаболическим синдромом. Российские медицинские вести. 2014;4:25-40.
- Pasarin M, Abraldes JG, Rodriguez-Vilarrupla A, LaMura V, Garcia-Pagan JC, Jaime Bosch J, Abraldes JG, Massimo Federici. Insulin resistance and liver microcirculation in a rat model of early NAFLD. J Hepatol. 2011;55:1095-1102.
- Wiest R, Groszmann RJ. The paradox of nitric oxide in cirrhosis and portal hypertension: too much, not enough. Hepatology. 2002;35:478-491.
- Langer DA, Das A, Semela D, Kang-Decker N, Hendrickson H, Bronk SF, Katusic ZS, Gores GJ, Shah VH. Nitric oxide promotes caspase-independent hepatic stellate cell apoptosis through the generation of reactive oxygen species. Hepatology. 2008;47:1983-1993.
- Ding BS, Nolan DJ, Butler JM, James D, Babazadeh AO, Rosenwaks Z, Mittal V, Kobayashi H, Shido K, Lyden D, Sato TN, Rabbany SY, Rafii S. Inductive angiocrine signals from sinusoidal endothelium are required for liver regeneration. Nature. 2010;468:310-315.
- Montagnani M, Chen H, Barr VA, Quon MJ. Insulin-stimulated activation of eNOS is independent of Ca2+ but requires phosphorylation by AktatSer (1179). J Biol Chem. 2001;276:30392-30398.
- Duncan ER, Crossey PA, Walker S, Anilkumar N, Poston L, Douglas G, Ezzat VA, Wheatcroft SB, Shah AM, Kearney MI. Effect of endothelium-specific insulin resistance on endothelial function in vivo. Diabetes. 2008;57:3307-3314.
- Pasarín M, LaMura V, Gracia-Sancho J, García-Calderó H, Rodríguez-Vilarrupla A, García-Pagán JC, Bosch J, Abraldes JG. Sinusoidal endothelial dysfunction precedes inflammation and fibrosis in a model of NAFLD. PLoS One. 2012;7(4):e32785.
- Биохимия. Под ред. Е.С. Северина. М.: Геотар-Мед; 2003.
- Оковитый С.В. Клиническая фармакология гепатопротекторов. ФАРМиндекс: Практик; 2002, вып. 3:33-58.
- Драпкина О.М. Компоненты метаболического синдрома: фокус на неалкогольную жировую болезнь печени. Справочник поликлинического врача. 2009;10:64-67.
- Драпкина О.М., Ивашкин В.Т. Неалкогольная жировая болезнь печени как компонент метаболического синдрома. Российские медицинские вести. 2010;2:72-79.
- Драпкина О.М., Деева Т.А., Попова И.Р. Неалкогольная жировая болезнь печени как облигатный признак ожирения. Российские медицинские вести. 2012;17(4):4-10.
- Драпкина О.М., Деева Т.А., Волкова Н.П. Современные подходы к диагностике и лечению неалкогольной жировой болезни печени. Терапевтический архив. 2014;10:116-123.
补充文件
![](/img/style/loading.gif)