Markers of Inflammation in Patients With Antiphospholipid Syndrome and Cardiovascular Pathology

Середавкина, Н. В.; Решетняк, Т. М.; Александрова, Е. Н.; Новиков, А. А.; Mach, E S; Новикова, Д. С.; Диатроптова, М. А.; Насонов, Евгений Львович

doi:10.14412/1995-4484-2010-729

Cited by 2 publications

(8 citation statements)

References 24 publications

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“…The attained results on increased concentrations of proinflammatory cytokines (IL1β, IL6, TNFα) in the serum of the experimental animals with APS conform with the literature [6,17,18]. According to N.V. Seredavkina [6], an increased concentration of IL6 and TNFα in the patients with APS compare to the control group was established. It is not clear whether aPL affect endothelial cells directly or through TNFα.…”

Section: Discussionsupporting

confidence: 81%

“…According to A. Farzaneh-Far et al [17], who investigated the levels of CRP IL 6, ISAM-1, pTNF αP2, pTNF αP2 in the patients with SLE, only increased pTNF αP1 and pTNF αP2 were asso ciated with aPL positivity. According to NV Seredavkin a negative correlation between CRP and IgG β2GP1 levels was established [6]. R.R.…”

Section: Discussionmentioning

confidence: 99%

“…It is established that increased concentrations of TNFα are associated with pregnancy miscarriage in APS [6,8], endotheliocytes activation, and chemokine amplification that leads to subendothelial leukocyte accumulation, endothelial dysfunction, microcirculation distur bances [16].…”

Section: Discussionmentioning

confidence: 99%

“…APS can be classified only in the presence of thrombotic (noninflam matory arterial, venous or small vessel thrombosis) obstetric complications (death of one or more morphologically normal fetus at or beyond the 10 th week of gestation; one or more premature birth of normal fetus before the 34 th week due to eclampsia, pre-eclampsia or placental insufficiency), or increased aPL level [2]. The mechanisms of thrombosis in APS have not been fully studied yet [6].…”

Section: Introductionmentioning

confidence: 99%

“…Cytokines, being synthesized at the inflammation site, affect virtually all cells invol ved in the inflammation development, as well as granulocytes, macrophages, fibroblasts, endothelial cells, epithelium cells, T and B lymphocytes [10].The inflammatory processes are controlled by the proinflammatory (IL1, IL2, IL6, IL8, IL12, TNFα, IFN) and anti inflammatory (IL4, IL10, TGF) cytokines [11]. Therefore, the study of pathobiochemical mechanisms of APS development, particularly establishment of the role of the cytokine system in development of this pathology, and search for effective methods of its treatment is an urgent and social issue [1,6,11,12].…”

Section: Introductionmentioning

confidence: 99%

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Impact of Nitric Oxide Synthesis Modulators on the Cytokines Profile in Experimental Antiphospholipid Syndrome

Yaremchuk¹,

Посохова²,

Kuzmak³

et al. 2020

IJMMR

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Background. Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of specific antibodies. Objective. The aim of the study was to investigate the effect of combined use of L-arginine and aminoguanidine on cytokine profile (IL-1β, IL-6, TNF-α, IL-4, IL-10) in experimental APS. Methods. The study was performed on BALB/c female mice. L-arginine (25 mg/kg) and aminoguanidine (10 mg/kg) were used for correction. Serum cytokines concentrations were assessed using an ELISA test. Results. It was found that in APS the concentration of proinflammatory cytokines IL-1β, IL-6 and TNF-a increases in 3.2, 2.3 and 4.5 times respectively, compare to the control. At the same time a decrease of the IL-4 and IL-10 in 1.9 and 2.2 times was evidenced. Aminoguanidine, a selective iNOS inhibitor, caused a significant decrease of TNF-α by 57% (p<0.001), but there were no changes in IL-1β, IL-6, IL-4 and IL-10 compare to the APS-group. L-arginine combined with aminoguanidine caused a significant decrease in the concentration of IL-1β by 30% (p<0.01), IL-6 – by 16% (p<0.05), TNF-a – by 59% (p<0.001) compare to the control. At the same time, the concentration of IL-4 increased by 35% (p <0.01), IL-10 – by 25% (p<0.005). Conclusions. Combined use of the precursor of the NO synthesis L-arginine and aminoguanidine, a selective iNOS inhibitor, leads to a decrease in the concentrations of IL-1β, IL-6, TNF-a and an increase of IL-4 and IL-10 compare to the group of the BALB/c mice with APS and the group of animals administered with aminoguanidine.

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