scholarly journals Arterial dysfunction and systemic inflammation in patients with bronchial asthma

2012 ◽  
Vol 9 (1) ◽  
pp. 42-49
Author(s):  
E A Sobko ◽  
A Y Kraposhina ◽  
O P Ischenko ◽  
I V Demko ◽  
A B Salmina ◽  
...  
Keyword(s):  
Asthma Control ◽  
Severe Asthma ◽  
Bronchial Asthma ◽  
Peripheral Blood ◽  
Vascular Wall ◽  
Control Group ◽  
External Respiration ◽  
Steroid Dependent ◽  
Healthy Donors ◽  
And Function

Background. The objective of this study was to estimate a vascular wall status of large arteries and function of endothelium in patients with different clinical forms of bronchial asthma throughout the disease progression. 220 patients with bronchial asthma have been examined, including 106 persons with moderate asthma ( 1 st group), 61 persons with severe asthma (2 nd group), and 53 persons with steroid-dependent asthma. Control group was formed from 40 healthy donors. Methods. We have assessed parameters of external respiration, arterial rigidity, and the levels of TNFα, IL-6, sCD31 (sPECAM-1), CRP in the peripheral blood at the time of exacerbation and 48 weeks later. Results. We found elevation of IL-6 and TNFα levels in all the tested groups in the period of exacerbation comparing to the control group (p

scholarly journals CYTOKINES PROFILE IN BLOOD IN SEVERE ASTHMA PATIENTS WITH OBESITY

2013 ◽  
Vol 10 (6) ◽  
pp. 13-19
Author(s):  
E A Sobko ◽  
I A Soloveva ◽  
O P Ischenko ◽  
A Y Kraposhina ◽  
I V Demko ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Bronchial Asthma ◽  
Systemic Inflammation ◽  
Peripheral Blood ◽  
Proinflammatory Cytokine ◽  
Control Group ◽  
Obese Patients ◽  
Asthma Patients ◽  
Ifn Γ ◽  
Inflammation Signs

Background. To study the cytokines profile in the peripheral blood of patients with severe asthma and obesity. Methods.139 patients with severe bronchial asthma have been examined, including 66 patients with severe bronchial asthma and body mass index (BMI) 30 (2nd group). The control group was formed from 40 healthy volunteers. The respiratory function, the cytokine integral index and the levels of TNFα, IL4, IL6, IL2, IL10, IFN-γ, IL8, IL17 in the peripheral blood of patients in and out of an exacerbation were studied. Results. More significant systemic inflammation signs expressed in increased levels of TNFα, IL6, IL4, IL2 and IFN-γ were found in exacerbation period of the disease. In obese patients the increased level of proinflammatory cytokine IL17 in exacerbation period was estimated. Conclusion. We have demonstrated the presence of systemic inflammation in patients with severe BA, regardless of the presence of obesity, increased level of proinflammatory cytokine IL17 in patients with severe bronchial asthma and obesity in the period of exacerbation. It can be a reason of the low effect of steroid therapy in patients with BMI >30.

scholarly journals Hyperexpression of TLR2 and TLR4 in patients with ischemic stroke in acute period of the disease

2020 ◽  
Vol 22 (4) ◽  
pp. 665-674
Author(s):  
L. V. Gankovskaya ◽  
L. V. Stakhovskaya ◽  
V. V. Grechenko ◽  
E. A. Koltsova ◽  
O. S. Uvarova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Innate Immunity ◽  
Ischemic Stroke ◽  
Peripheral Blood ◽  
Surface Expression ◽  
Control Group ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Healthy Donors ◽  
Tlr4 Gene

Pathogenesis of ischemic stroke  is actively  involved  in the  system  of innate immunity. Under conditions of cerebral  ischemia, a number of biologically  active  substances are  released  that  interact with innate immunity receptors, in particular TLR2  and  TLR4, which  exacerbate inflammation in brain  tissue. Identification of predictor markers  at the level of the innate immunity system may foresee the clinical course of ischemic stroke and ensure timely treatment. Our objective was to study expression of TLR2 and TLR4 receptors in peripheral blood leukocytes  in patients with ischemic stroke in the dynamics of the disease. 27 people  were included in the study. The main  group consisted of patients with ischemic stroke of varying severity (n = 19). Patients of the main  group were divided into two subgroups:  with an NIHSS index value of < 10 (n = 10) and > 10 (n = 9). The control group included healthy  donors  with no history  of acute  and chronic inflammatory diseases (n = 8). Peripheral blood  leukocytes  were used as the  test material. To determine expression  of the TLR2  and TLR4  genes, RT-PCR in real time was used. Surface  expression  of TLRs was determined by flow cytometry. A study of the TLR2 and TLR4 gene expression showed that on the 1st, 3rd  and 7th  day post-stroke, the TLR4 gene expression  in patients was significantly  increased, when compared to the control group (p < 0.01), whereas TLR2 gene expression on the 3rd  day of the disease was not statistically different from the control group. A study of surface expression  of receptors showed that the average TLR2 fluorescence intensity on the patients’ peripheral blood monocytes was significantly  increased on the 1st  and 3rd  day of disease when compared to the control group.  The  surface  expression  of TLR4  on monocytes has a statistically significant  increase  only on day 7. Assessment  of surface expression  of TLRs in subgroups  with different  severity values by NIHSS showed that  patients with a NIHSS index > 10 had a significantly  higher  level of surface of TLR2  expression  over the observation period, while the largest difference in TLR4  expression  in the subgroups  was observed  on the 1st day of the disease (p < 0.05). Patients with ischemic stroke showed an increase  in TLR2 and TLR4 expression at the gene and protein level, compared to healthy  donors. These indices can be considered possible predictors for clinical  prognosis  of ischemic stroke.

scholarly journals Effects of the Airway Obstruction on the Skin Microcirculation in Patients with Bronchial Asthma

2016 ◽  
Vol 71 (3) ◽  
Author(s):  
Irina V. Tikhonova ◽  
N. I. Kosyakova ◽  
A. V. Tankanag ◽  
N. K. Chemeris
Keyword(s):  
Blood Flow ◽  
Airway Obstruction ◽  
Bronchial Asthma ◽  
Skin Blood Flow ◽  
Peripheral Blood ◽  
Atopic Asthma ◽  
Control Group ◽  
Bronchial Obstruction ◽  
Peripheral Blood Flow ◽  
Flow Parameters

Background: Pulmonary hemodynamic disorders depend on the inflammatory phases and severity of the obstructive syndrome. However, the effect of asthma bronchial obstruction on the state of peripheral hemodynamics remains insufficiently known. Aims: To study the effects of airway obstruction on skin blood flow parameters and its regulatory systems in patients with persistent atopic bronchial asthma in the remission state.Materials and methods: A comparative study of the skin peripheral blood flow in patients with bronchial asthma with severe airway obstruction (1st group) and without obstruction (2nd group) was conducted. 20 patients with confirmed diagnosis of atopic asthma of 50–74 years old participated in the study. All patients received basic therapy in a constant dosing of high doses of inhaled glucocorticosteroids/long-acting beta-2-agonists. The control group included 20 healthy volunteers without evidence of bronchial obstruction. The study lasted for 3 months. The forced expiratory volume in 1 s (FEV1) was used to evaluate the bronchial obstruction by spirometry technique. Skin blood perfusion changes were recorded by laser Doppler flowmetry at rest and in response to short-term local ischemia. Registered peripheral blood flow signals were examined using the amplitude temporal filtering in five frequency intervals to identify the functional features of the peripheral blood flow regulation systems. Results: Consistent two-fold decrease of the oscillation amplitudes was found in the neurogenic interval at rest (p=0.031), as well as in the myogenic (p=0.043; p=0.031) and endothelial intervals (p=0.037; p≤0.001) both at rest and during the postocclusive reactive hyperemia respectively in the 1st group of patients with bronchial obstruction (FEV1 80%) compared with the control group. No significant changes were revealed for skin blood flow parameters in the 2nd patient group (without obstruction, FEV1 80%) in comparison to control subjects.Conclusions: The presence of bronchial obstruction has a significant impact on the changes of the amplitudes of skin blood flow oscillations in patients with bronchial asthma in the myogenic, neurogenic and endothelial intervals.

scholarly journals Impact of Berberine on the Expression of Apollon Gene in Chronic Lymphocytic Leukemia

2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Niloofar Ghanizade ◽  
Maral Hemati ◽  
Habib Jaafarinejad ◽  
Mehrnoosh Pashaei ◽  
Parviz Kokhaei
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Lymphocytic Leukemia ◽  
Control Group ◽  
Peripheral Blood Mononuclear ◽  
Healthy Donors ◽  
Blood Mononuclear Cells ◽  
The Impact

Background: The incidence of B-chronic lymphocytic leukemia (B-CLL) resulting from the clonal accumulation of apoptosis-resistant malignant B lymphocytes is growing in the adult population of Iran. Inhibitors of apoptosis proteins (IAPs) are considered as factors that can delay the onset of CLL cell apoptosis. Berberine is an isoquinoline alkaloid isolated from Cotridis rhizoma that exhibits anti-tumor activities through various mechanisms. Objectives: In this study, we investigated the impact of berberine on the level of Apollon expression in peripheral blood mononuclear cells (PBMCs) of 12 cases newly diagnosed with CLL and 6 healthy donors. Methods: At first, the level of Apollon expression was assessed in PBMCs of CLL patients compared to the healthy donors. Peripheral blood mononuclear cells were cultured in RPMI-1640 medium with 5% fetal bovine serum (FBS) and 1% penicillin/streptomycin for 48 hours, and the effect of berberine (25 µM) on the level of Apollon expression in CLL patients was assessed and compared to that of healthy donors. Results: We found that the expression level of Apollon was not significantly different between CLL patients and healthy donors (P = 0.640). Moreover, berberine induced no significant differences in Apollon expression as compared to the untreated (control) group (P = 0.545 and P = 0.267 in CLL patients and healthy donors, respectively). Conclusions: Overall, our results suggest that berberine has no direct effect on the expression of Apollon gene in CLL patients, and pro-apoptotic impacts of berberine may be exerted through other mechanisms.

Effect of Nitrogen Oxide on the Gums Lamina propria Structure and Function in the Experimental Gastritis, Duodenitis and Pharmacological Correction

2017 ◽  
Vol 30 ◽  
pp. 86-96
Author(s):  
Y.G. Romanenko ◽  
V.I. Mamchur ◽  
A.E. Levykh
Keyword(s):  
Nitrogen Oxide ◽  
Lamina Propria ◽  
Vascular Wall ◽  
Structure And Function ◽  
Control Group ◽  
Blood Plasma Proteins ◽  
Wall Permeability ◽  
And Function ◽  
The Given ◽  
Experimental Group

In the conditions of experi mental chronic gastritis and duodenitis reproduction, carried out among Wistar line 24 rats, was investigated effect of the nitrogen oxide stable metabolites content in the gums homogenates on a lamina propria structure and function. Results of our research have been shown, that level of nitrogen oxide stable metabolites in the rats’ gums tissues homogenates with gastritis and duodenitis decreased in three times, compared with a same period at the intact animals, which indicated about depletion of a nitrogen oxide depot at the given disease. It was revealed a significant decrease typical for the protein and glycoprotein content in the animals gums tissues at the experimental group, which indicated about the catabolic processes predominance. Amount of hexosamines in the gums was significantly increased, which was correlated with a morphological picture (gums lamina propria impregnation with the blood plasma proteins), testified about a change in the vascular wall permeability and microcirculation disruption. In the animals from experimental group was reduced a height of gums papillae connective tissue to 27.18±1.86 x 10-6 m against 56.93±2.64 x 10-6 m in the rats from control group. In the gums lamina propria defines phenomenon of the papillary and reticular layer fibrosis. After medicamentous correction, carried out with an antioxidant and the nitrogen oxide donor was observed repairing structure of the gums lamina propria on a background of increasing microvasculature area. It was determined significantly increased protein and glycoprotein content in the gums tissues with increased levels of nitrogen oxide metabolites.

scholarly journals Integrative indicators of anti-endotoxin immunity and systemic inflammation in bronchial asthma patients with different inflammatory phenotypes

2020 ◽  
pp. 58-64
Author(s):  
В.А. Белоглазов ◽  
Ю.О. Попенко ◽  
Н.А. Шадчнева ◽  
А.И. Гордиенко ◽  
В.Б. Калиберденко ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Systemic Inflammation ◽  
Peripheral Blood ◽  
Induced Sputum ◽  
Control Group ◽  
C Reactive Protein ◽  
Blood Concentrations ◽  
Reactive Protein ◽  
Inflammatory Phenotypes

Актуальность. Поскольку роль эндотоксина в индукции бронхообструктивного синдрома сегодня уже не вызывает сомнений, представляется целесообразным и определение роли антиэндотоксинового иммунитета (АЭИ) в формировании различных биофенотипов хронического воспаления, которые лежат в основе особенностей течения бронхиальной астмы (БА). Цель настоящего исследования - определение роли гуморального и мукозального звеньев АЭИ и системного воспаления при различных биофенотипах воспаления у больных БА, которые могли бы быть полезны для разработки персонифицированной терапии. Материалы и методы. В исследование включены 109 больных с верифицированным диагнозом среднетяжёлой и тяжёлой бронхиальной астмы. Пациенты были разделены на 3 группы в зависимости от типа воспаления в дыхательных путях: 1-я группа - эозинофильный, 2-я группа - нейтрофильный, 3-я группа - смешанный гранулоцитарный. Гуморальное и мукозальное звенья эндотоксин-связывающих систем оценивали по уровням специфических эндотоксин-связывающих антител классов M, A, G (анти-ЭТ IgM, анти-ЭТ IgA, анти-ЭТ IgG) в периферической крови, и уровню секреторного антиэндотоксинового иммуноглобулина класса A в индуцированной мокроте. Системное воспаление оценивали по концентрации С-реактивного белка (СРБ). Результаты. При нейтрофильном и смешанном биофенотипах воспаления зарегистрированы повышенные уровни анти-ЭТ IgM и анти-ЭТ IgА в периферической крови. В то время как при эозинофильном биофенотипе воспаления не выявлено существенных различий данных показателей от контрольной группы. Концентрация анти-ЭТ IgG во всех группах больных бронхиальной астмы не отличалась от диапазона нормы. При всех биофенотипах воспаления выявлено повышение концентраций секреторного анти-ЭТ IgА и СРБ в рамках низкоинтенсивного воспаления. Наибольший уровень анти-ЭТ IgА и СРБ зарегистрирован при нейтрофильном и смешанном биофенотипах воспаления. Выявлены умеренные прямые корреляционные связи: между уровнем секреторного анти-ЭТ IgA и относительным количеством нейтрофилов в индуцированной мокроте (r = 0,469, р < 0,05); между уровнем СРБ и уровнем секреторного анти-ЭТ IgA (r = 0,427, р < 0,05). Выводы. Наиболее выраженный гуморальный и мукозальный ответ на эндотоксин и интенсивность системного воспаления при нейтрофильном и смешанном биофенотипах воспаления свидетельствуют о значительной роли ингаляционного эндотоксина в формировании тяжёлой астмы. Выявленный дисбаланс гуморального и мукозального звеньев АЭИ систем дополняет современные представления патогенеза бронхиальной астмы с различными биофенотипами воспаления, предоставляет перспективу возможности персонификации лечения и достижения контроля заболевания. Background. Since the role of endotoxin in induction of broncho-obstructive syndrome is above any doubt today, we focused on the role of anti-endotoxin immunity (AEI) in the formation of different phenotypes of chronic inflammation, which underlie characteristics of the course of asthma. The aim of this study was to determine the role of humoral and mucosal components of AEI and systemic inflammation in different inflammatory phenotypes in patients with asthma, which could be useful in developing personalized therapy. Materials and methods. The study included 109 patients with a verified diagnosis of moderate to severe asthma. All patients were divided into 3 groups depending on the type of inflammation in the respiratory tract: Group 1, eosinophilic; Group 2, neutrophilic; and Group 3, mixed granulocytic inflammation. The humoral and mucosal components of endotoxin binding systems were evaluated by levels of specific endotoxin-binding class M, A, and G antibodies (anti-ET IgM, anti-ET IgA, and anti-ET IgG) in peripheral blood and the level of secretory anti-endotoxin IgA in induced sputum. Systemic inflammation was assessed by concentration of C-reactive protein (CRP). Results. Peripheral blood concentrations of anti-ET IgM and anti-ET IgA were elevated in neutrophilic and mixed inflammatory phenotypes. At the same time, in the eosinophilic inflammatory phenotype, these indexes were not significantly different from the control group. In all groups of patients with asthma, concentrations of anti-ET IgG were similar and remained within the normal range. In all inflammatory phenotypes, concentrations of secretory anti-ET IgA and C-reactive protein were increased within the range of low-intensity inflammation. The highest levels of anti-ET IgA and CRP were found in neutrophilic and mixed inflammatory phenotypes. Levels of secretory anti-ET IgA moderately directly correlated with the relative number of neutrophilic leukocytes in induced sputum (r = 0.469, р < 0.05) and levels of CRP moderately directly correlated with levels of secretory anti-ET IgA (r = 0.427, р < 0.05). Conclusions. The most pronounced humoral and mucosal response to endotoxin and the intensity of systemic inflammation in neutrophilic and mixed inflammatory phenotypes evidenced a significant role of inhaled endotoxin in the formation of severe asthma. The observed imbalance of humoral and mucosal components in AEI systems supports modern ideas of the pathogenesis of asthma with different inflammatory phenotypes and provides a promising possibility of individualized treatment and control of the disease.

scholarly journals Association of FOXP3 gene -3279 C>A polymorphism with the risk of pulmonary sarcoidosis

2017 ◽  
Vol 89 (12) ◽  
pp. 64-67 ◽  
Author(s):  
I E Malysheva ◽  
L V Topchieva ◽  
E L Tikhonovich ◽  
I V Kurbatova ◽  
O V Balan
Keyword(s):  
Peripheral Blood ◽  
Polymorphic Marker ◽  
Pulmonary Sarcoidosis ◽  
Control Group ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Foxp3 Gene ◽  
Healthy Donors ◽  
Gene Transcripts ◽  
The Republic

Aim. To investigate the association of the polymorphic marker -3279 C>A of the FOXP3 gene with the risk of pulmonary sarcoidosis (PS) and to estimate the transcription level of this gene in the carriers of different genotypes of this polymorphic marker. Subjects and methods. The investigation included 99 patients of Russian ethnicity (mean age, 45.41±1.31 years) living in the Republic of Karelia, who were diagnosed with persistent PS, and 116 healthy donors (mean age, 42.06±1.30 years) in the control group. The alleles and genotypes of the polymorphic marker -3279 C>A of the FOXP3 gene were identified using polymerase chain reaction (PCR)-restriction fragment length polymorphism. The number of transcripts of the studied gene in the peripheral blood leukocytes of healthy donors and PS patients was determined with real-time PCR. Results. The control group and the PS patient one had no statistically significant differences in the distribution of the frequencies of alleles and genotypes by the polymorphic marker –308G>A of the FOXP3 gene (p > 0.05). The number of FOXP3 gene transcripts was not statistically significantly different in the peripheral blood leukocytes of patients with PS and control individuals. No statistically significant differences were observed in the mRNA expression levels in the above-mentioned gene in the carriers of different genotypes by the polymorphic marker -3279 C>A of the FOXP3 gene in all examined groups. Conclusion. The polymorphic marker -3279 C>A of the FOXP3 gene is unassociated with the risk of PS.

scholarly journals The characteristics of serum circulating immune complexes of patients with atopic asthma with different severity degree

2013 ◽  
Vol 94 (5) ◽  
pp. 744-748 ◽  
Author(s):  
Y V Skibo ◽  
N S Kurmaeva ◽  
V N Tsibulkina ◽  
I G Mustafin ◽  
Z I Abramova
Keyword(s):  
Severe Asthma ◽  
Bronchial Asthma ◽  
Immune Complexes ◽  
Wave Length ◽  
Molecular Complexes ◽  
Electrophoretic Analysis ◽  
Circulating Immune Complexes ◽  
Atopic Asthma ◽  
Control Group ◽  
Serum Samples

Aim. To evaluate the serum level of pathogenic circulating immune complexes in patients with mild and severe atopic bronchial asthma. Methods. Serum samples of patients with atopic asthma of mild persistent (30 patients) and severe persistent (20 patients) forms were analyzed. The control group consisted of 15 healthy volunteers. To detect the giant, large, medium and small-sized serum immune complexes, 3, 3.5, 4 and 7% polyethyleneglycol-6000 solutions were used. For quantitative evaluation of the immune complexes we measured the ultraviolet optical density at 280 nm wave length. To separate the immune complexes from immunoglobulin, Protein-G-Sepharose was used. Determination of the protein composition of circulating immune complexes was performed by electrophoresis in 8% polyacrylamide gel. Results. The concentration of immune complexes was increased in patients with bronchial asthma compared to healthy donors. Small and medium-sized immune complexes were prevailing, their concentrations correlated with the severity of asthma. Large, medium and small-sized immune complexes participated in immunopathological reactions in patients with both mild and severe asthma, with immune complexes pathogenicity coefficient significantly increased depending on the severity of the disease. Electrophoretic analysis of circulating immune complexes has shown the presence of proteins with molecular weight of 60 kDa in the complexes of all sizes. In the severe asthma group, an antigen fraction with a molecular mass of 36 kDa within the small-sized molecular complexes was revealed. Conclusion. The observed increase of small and medium-sized circulating immune complexes serum levels in patients with bronchial asthma may be an indicator of of these patients predisposal to autoimmune reactions development.

scholarly journals The role of IL-5 in eosinophils’ apoptotic death mechanisms in patients with bronchial asthma

2003 ◽  
Vol 2 (2) ◽  
pp. 38-43
Author(s):  
I. I. Ivanchuk ◽  
A. E. Sazonov ◽  
F. I. Petrovsky ◽  
I. S. Lescheva ◽  
A. P. Kopieva ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Bronchial Asthma ◽  
Peripheral Blood ◽  
Potential Role ◽  
Healthy Donors ◽  
Apoptotic Activity ◽  
Blood Eosinophils ◽  
Cellular Destruction ◽  
Stimulation Of

Investigations of the mRNA expression of apoptosis intracellular regulators, bcl-2 and bcl-xL antagonists and bax, bcl-xL agonists of cellular destruction as well as mRNA expression of IL-5 were carried out. As a result of investigation of potential role of IL-5 in the regulation of programmable bcl-2-dependent destruction we found the increase of vitality and mRNA expression stimulation of bcl-2 peripheral blood eosinophils in patients with bronchial asthma (BA). It was found that fresh-isolated peripheral blood eosinophils in all investigated groups expressed bax and bcl-xL mRNA, bcl-xS had the less activity. In peripheric blood eosinophils of healthy donors the bcl-2 expression was not found, however, the increase of mRNA expression by IL-5 was shown in group of patients with bronchial asthma and, possibly connected with this, the appearance of bcl-2 activity. Thus, the decrease of apoptotic activity in peripheral blood eosinophils in patients with bronchial asthma may lead to the increase of eosinophil portion that is subjected to necrotic destruction and this may significantly contribute into bronchial asthma pathogenesis.

scholarly journals Garlic Extract (Allicin) Improves the Proliferation of Endothelial Progenitor Cell (EPC) from Patients with Stable Coronary Artery Disease

2020 ◽  
Vol 8 (A) ◽  
pp. 65-69
Author(s):  
Yudi Her Oktaviono ◽  
Budi Susetyo Pikir ◽  
Fatimah Alzahra ◽  
Makhyan Jibril Al-Farabi ◽  
Alisia Yuana Putri
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Progenitor Cell ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Stable Coronary Artery Disease ◽  
Immunohistochemical Method ◽  
Control Group ◽  
Artery Disease ◽  
And Function

BACKGROUND: The reduced number and function of endothelial progenitor cell (EPC) in stable coronary artery disease (SCAD) patients aggravate endothelial dysfunction and inhibit neovascularization, thus lead to atherosclerosis. Garlic is currently believed to increase the number and function of EPC. AIM: Therefore, this in vitro study was conducted to analyze the effect of garlic extract (allicin) on the proliferation of EPC in patients with SCAD. METHODS: Mononuclear cells were isolated from peripheral blood of eight SCAD patients and cultured on colony-forming unit (CFU)-Hill medium for 3 days. Samples were divided into two groups: Group treated with allicin and control group. The treatment group was then divided into three subgroups which received 10, 50, and 100 mg/ml of doses and incubated for 48 h. EPC proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay. Immunohistochemical method of CD34+ was performed for EPC identification. Data were analyzed using independent t-test and ANOVA. RESULTS: MTT assay showed a significant increase in EPC proliferation in the allicin group compared to the control group (0.2811 ± 0.008 vs. 0.194 ± 0.151, p < 0.05) and significant improvements were observed in each dose increment. CFU-Hill quantification shows the addition of EPC colony in high-dose allicin. Immunohistochemical method shows positive CD34+ expression. CONCLUSION: Allicin increases EPC proliferation dose-dependently from peripheral blood of SCAD patients.

Sign in / Sign up

Export Citation Format

Share Document