Abstract 299: Natural Product Derivative Bio Promotes Recovery After Myocardial Infarction via Unique Modulation of the Cardiac Microenvironment

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Yong Sook Kim ◽  
Wan Seok Kang ◽  
Ju Hee Kang ◽  
Youngkeun Ahn
Keyword(s):  
Myocardial Infarction ◽  
Glycogen Synthase ◽  
Cardiac Fibroblasts ◽  
Serum Levels ◽  
Interleukin 10 ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
Cardiomyocyte Proliferation ◽  
Related Factors ◽  
Anti Inflammatory

Rationale: Myocardial infarction (MI) induces cardiac remodeling, which is regulated by the cardiac microenvironment and results in scarring and loss of cardiac function. Targeting the microenvironment represents a novel therapeutic approach. Objective: To investigate the therapeutic effect of a natural compound derivative, BIO [(2’Z,3’E)-6-Bromoindirubin-3′-oxime], on cardiac microenvironment cells and remodeling post-MI. Methods and Results: Using a series of co-culture studies, BIO was shown to induce proliferation in cardiomyocytes and, conversely, inhibit proliferation in cardiac fibroblasts. In addition, BIO produced anti-fibrotic effects in the fibroblasts, such as reduced motility and expression changes in fibrosis-related factors. In macrophages, BIO inhibited the expression of pro-inflammatory inducible nitric oxide synthase. Interestingly, BIO modulated molecular crosstalk between cardiac fibroblasts and differentiating macrophages to increase expression of anti-inflammatory M2 macrophage markers. In the optically transparent zebrafish-based model of heart failure, BIO induced cardiomyocyte proliferation to recover survival rate. BIO is a known glycogen synthase kinase-3β inhibitor, but these effects could not be recapitulated using the classical inhibitor, lithium chloride; indicating novel, potential therapeutic effects of BIO on remodeling. We characterized these novel effects of BIO as differential modulation of p27 expression and potent induction of interleukin-10 in microenvironment cells. In rat MI model, BIO reduced fibrosis and improved cardiac performance. Histological analysis revealed a greater presence of anti-inflammatory M2 macrophages in the infarction zone. BIO treatment also reduced serum levels of pro-fibrotic interleukin-6. Conclusions: BIO differentially activates signaling pathways in cardiomyocytes, cardiac fibroblasts and cardiac macrophages to reduce fibrosis, increase cardiomyocyte proliferation and promote recovery post-MI.

scholarly journals Hypoxia impairs mesenchymal stromal cell-induced macrophage M1 to M2 transition

TECHNOLOGY ◽  
2017 ◽  
Vol 05 (02) ◽  
pp. 81-86 ◽  
Author(s):  
Renea A. Faulknor ◽  
Melissa A. Olekson ◽  
Emmanuel C. Ekwueme ◽  
Paulina Krzyszczyk ◽  
Joseph W. Freeman ◽  
...  
Keyword(s):  
Wound Healing ◽  
Chronic Wounds ◽  
Interleukin 10 ◽  
M2 Macrophage ◽  
Therapeutic Effects ◽  
M1 Macrophages ◽  
Normal Wound Healing ◽  
Hypoxic Environment ◽  
Anti Inflammatory ◽  
M2 Phenotype

The transition of macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype is crucial for the progression of normal wound healing. Persistent M1 macrophages within the injury site may lead to an uncontrolled macrophage-mediated inflammatory response and ultimately a failure of the wound healing cascade, leading to chronic wounds. Mesenchymal stromal cells (MSCs) have been widely reported to promote M1 to M2 macrophage transition; however, it is unclear whether MSCs can drive this transition in the hypoxic environment typically observed in chronic wounds. Here we report on the effect of hypoxia (1% O[Formula: see text] on MSCs’ ability to transition macrophages from the M1 to the M2 phenotype. While hypoxia had no effect on MSC secretion, it inhibited MSC-induced M1 to M2 macrophage transition, and suppressed macrophage expression and production of the anti-inflammatory mediator interleukin-10 (IL-10). These results suggest that hypoxic environments may impede the therapeutic effects of MSCs.

scholarly journals Effect of probiotic supplementation along with calorie restriction on metabolic endotoxemia, and inflammation markers in coronary artery disease patients: a double blind placebo controlled randomized clinical trial

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Jalal Moludi ◽  
Hossein Samadi Kafil ◽  
Shaimaa A. Qaisar ◽  
Pourya Gholizadeh ◽  
Mohammad Alizadeh ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Lactobacillus Rhamnosus ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Probiotic Supplementation ◽  
Related Factors ◽  
Double Blind ◽  
Artery Disease ◽  
Metabolic Endotoxemia

Abstract Purpose Alterations in the gut microbiome (dysbiosis) has been associated with increased microbial translocation, leading to chronic inflammation in coronary artery disease (CAD). It has been proposed that modulation of gut microbiota by probiotic might modify metabolic endotoxemia. Therefore, the purpose of this study was to examine the effects of Lactobacillus rhamnosus GG (LGG) on endotoxin level, and biomarkers of inflammation in CAD participants. Methods This study was a 12-weeks randomized, double-blind, and intervention on 44 patients with CAD. Patients were randomly allocated to receive either one LGG capsule 1.6 × 109 colony-forming unit (CFU) or the placebo capsules for 12 weeks. In addition, all the participants were also prescribed a calorie-restricted diet. Serum levels of interleukin-1β (IL-1β), Toll-like receptor 4 (TLR4), interleukin-10 (IL-10), and lipopolysaccharide (LPS), were assessed before and after the intervention. Results A significant decrease in IL1-Beta concentration (− 1.88 ± 2.25, vs. 0.50 ± 1.58 mmol/L, P = 0.027), and LPS levels (− 5.88 ± 2.70 vs. 2.96+ 5.27 mg/L, P = 0.016), was observed after the probiotic supplementation compared with the placebo. Participants who had ≥2.5 kg weight loss showed significantly improved cardiovascular-related factors, compared to patients with < 2.5 kg weight reduction, regardless of the supplement they took. Conclusion These data provide preliminary evidence that probiotic supplementation has beneficial effects on metabolic endotoxemia, and mega inflammation in participants with CAD.

Association of interleukin-10 promoter polymorphisms with serofast state after syphilis treatment

2018 ◽  
Vol 95 (3) ◽  
pp. 163-168 ◽  
Author(s):  
Maciej Pastuszczak ◽  
Bogdan Jakiela ◽  
Anna Wojas-Pelc
Keyword(s):  
Immune Response ◽  
Interleukin 10 ◽  
Control Group ◽  
Serological Response ◽  
Promoter Polymorphisms ◽  
Related Factors ◽  
Adequate Treatment ◽  
Early Syphilis ◽  
Inflammatory Immune Response ◽  
Anti Inflammatory

ObjectivesRecent studies suggested that upregulation of anti-inflammatory immune response during early syphilis may be associated with persistence of Treponema pallidum infection despite adequate treatment, resulting in a serofast state. The objective of this study was to determine whether enhanced interleukin (IL)-10-related response during early T. pallidum infection increased the risk of serofast syphilis.MethodsTwo IL10 gene promoter polymorphisms affecting IL-10 production (−1082A>G [rs1800896], −592C>A [rs1800872]) and serum levels of IL-10 were measured in 80 patients with early syphilis before and 6 months after penicillin treatment and in 24 healthy volunteers (control group).ResultsAfter 6 months, patients were stratified based on serological response into two groups: (1) serofast state (n = 28) and (2) serologically cured (n = 52). Pretreatment and post-treatment serum IL-10 levels were significantly higher in patients who remained serofast compared with those who had a serological cure (p<0.001). The GG genotype of the −1082A>G (rs1800896) polymorphism and the CC genotype of the −592C>A (rs1800872) polymorphism were significantly correlated with higher serum IL-10 levels. Moreover, the OR for remaining serofast for carriers of these genotypes was 16.2 (95% CI: 4.1 to 65.0, p<0.0001) and 2.9 (95% CI: 1.4 to 5.9, p=0.002), respectively.ConclusionsWe showed that a pronounced anti-inflammatory immune response may be an important predictor for the serofast state. Additionally, host-related factors such as polymorphisms of immune regulatory genes may influence the risk of remaining serofast after syphilis therapy.

scholarly journals Role of Luteolin-Induced Apoptosis and Autophagy in Human Glioblastoma Cell Lines

Medicina ◽  
2021 ◽  
Vol 57 (9) ◽  
pp. 879 ◽  
Author(s):  
Hye-Sung Lee ◽  
Bong-Soo Park ◽  
Hae-Mi Kang ◽  
Jung-Han Kim ◽  
Sang-Hun Shin ◽  
...  
Keyword(s):  
Cell Lines ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Glioblastoma Cell ◽  
Related Factors ◽  
Green Pepper ◽  
Real Time Quantitative Pcr ◽  
Anti Inflammatory ◽  
Induced Apoptosis ◽  
Glioblastoma Cell Lines

Background and Objectives: Malignant glioblastoma (GBM) is caused by abnormal proliferation of glial cells, which are found in the brain. The therapeutic effects of surgical treatment, radiation therapy, and chemo-therapy against GBM are relatively poor compared with their effects against other tumors. Luteolin is abundant in peanut shells and is also found in herbs and other plants, such as thyme, green pepper, and celery. Luteolin is known to be effective against obesity and metabolic syndrome. The anti-inflammatory, and anti-cancer activities of luteolin have been investigated. Most studies have focused on the antioxidant and anti-inflammatory effects of luteolin, which is a natural flavonoid. However, the association between the induction of apoptosis by luteolin in GBM and autophagy has not yet been investigated. This study thus aimed to confirm the occurrence of luteolin-induced apoptosis and autophagy in GBM cells and to assess their relationship. Materials and Methods: A172 and U-373MG glioblastoma cell lines were used for this experiment. We confirmed the apoptosis effect of Luteolin on GBM cells using methods such as 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence, Flow cytometry (FACS) western blot, and real-time quantitative PCR (qPCR). Results: In the luteolin-treated A172 and U-373MG cells, cell viability decreased in a concentration- and time-dependent manner. In addition, in A172 and U-373MG cells treated with luteolin at concentrations greater than 100 μM, nuclear fragmentation, which is a typical morphological change characterizing apoptosis, as well as fragmentation of caspase-3 and Poly (ADP-ribose) polymerase (PARP), which are apoptosis-related factors, were observed. Autophagy was induced after treatment with at least 50 μM luteolin. Inhibition of autophagy using 3MA allowed for a low concentration of luteolin to more effectively induce apoptosis in A172 and U-373MG cells. Conclusions: Results showed that luteolin induces apoptosis and autophagy and that the luteolin-induced autophagy promotes cell survival. Therefore, an appropriate combination therapy involving luteolin and an autophagy inhibitor is expected to improve the prognosis of GBM treatment.

scholarly journals Involvement of Interleukin-10 in the Anti-Inflammatory Effect of Sanyinjiao (SP6) Acupuncture in a Mouse Model of Peritonitis

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Morgana Duarte da Silva ◽  
Giselle Guginski ◽  
Maria Fernanda de Paula Werner ◽  
Cristiane Hatsuko Baggio ◽  
Rodrigo Marcon ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Interleukin 10 ◽  
Sham Acupuncture ◽  
Therapeutic Effects ◽  
Plasma Extravasation ◽  
Sterile Saline ◽  
Cell Counts ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Inflammatory Effect

In this study, we determined the anti-inflammatory effect of manual acupuncture at the Sanyinjiao or Spleen 6 (SP6) point on carrageenan-induced peritonitis in mice and investigated mechanisms that may underlie this effect. In the first set of experiments, male Swiss mice were allocated into five groups: the control (sterile saline), dexamethasone (DEXA), invasive sham-acupuncture (non-acupoint), SP6 acupuncture and carrageenan-treated groups. Ten minutes after needle retention or 30 min after DEXA treatment, mice received an intraperitoneal injection of carrageenan (750 μg/mouse). After 4 h, total leukocyte and differential cell counts (neutrophils and mononuclear), myeloperoxidase (MPO) activity, vascular permeability and cytokine levels were evaluated. In another set of experiments, adrenalectomized (ADX) mice were used to study the involvement of the adrenal gland on the therapeutic effects of acupuncture. Mice were allocated into two groups: the ADX and sham-operated animals (Sham ADX) that were subdivided into four subgroups each: the control (sterile saline), DEXA, SP6 acupuncture and carrageenan-treated groups. The SP6 and DEXA treatments inhibited the inflammatory cell infiltration, vascular permeability and MPO activity in carrageenan-injected mice. In addition, the SP6 treatment also increased interleukin (IL)-10 levels. In contrast, when the animals were adrenalectomized, the SP6 treatment failed to reduce total leukocyte and the plasma extravasation. In conclusion, this study clearly demonstrates the anti-inflammatory effect of SP6 acupuncture in a model of carrageenan-induced peritonitis. Our results demonstrated that SP6 acupuncture depends of the adrenal glands and increased IL-10 levels to produce its anti-inflammatory action.

Role of Pro-/Anti-Inflammatory Cytokines and their Correlation with Established Risk Factors in South Indians with Coronary Artery Disease

Angiology ◽  
2008 ◽  
Vol 60 (4) ◽  
pp. 419-426 ◽  
Author(s):  
Medha Rajappa ◽  
S. K. Sen ◽  
Alpana Sharma
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Unstable Angina ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Anti Inflammatory ◽  
Artery Disease

Cytokines are responsible for the modulation of immunological and inflammatory processes and play a significant role in the pathogenesis of coronary artery disease. We estimated the levels of pro-/anti-inflammatory cytokines in South Indian patients with coronary artery disease. The study population comprised of groups 1–3: 100 patients each with acute myocardial infarction, unstable angina, and stable angina, respectively, and group 4 (100 healthy controls). Cytokine levels (interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-α) were estimated by enzyme-linked immunosorbent assay (ELISA). Interleukin-6, interleukin-8, and tumor necrosis factor-α levels were significantly higher in patients from groups 1 and 2, than in group 3 and controls. Acute myocardial infarction patients exhibited higher serum levels of interleukin-10 compared with other groups and control subjects. Patients with unstable angina had significantly lower interleukin-10 concentrations than those with stable angina. The ratios of pro-/anti-inflammatory cytokines in all the study groups increased significantly when patients with unstable angina were compared to other groups. In patients with acute myocardial infarction, interleukin-10 and tumor necrosis factor-α levels showed significant correlation with established risk factors such as body mass index, blood pressure, and lipid levels. Acute myocardial infarction patients show elevation in proinflammatory and anti-inflammatory cytokines, while unstable angina is associated with low levels of serum interleukin-10. Higher levels of antiinflammatory cytokine interleukin-10 may be needed to provide protection in unstable angina. These cytokines are markers of coronary artery disease and may be used for the identification of high-risk patients with unstable angina/acute myocardial infarction.

scholarly journals Anti-inflammatory response of IL-4, IL-10 and TGF-β in patients with systemic inflammatory response syndrome

2000 ◽  
Vol 9 (3-4) ◽  
pp. 193-195 ◽  
Author(s):  
Donato Torre ◽  
Roberto Tambini ◽  
Silvana Aristodemo ◽  
Giovanna Gavazzeni ◽  
Antonio Goglio ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Systemic Inflammatory Response ◽  
Interleukin 4 ◽  
Significant Difference ◽  
Anti Inflammatory

The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a large number of clinical infective and noninfective conditions.The aim of this study was to investigate the role of anti-inflammatory cytokines such as interleukin–4 (IL–4), interleukin–10 (IL–10), and transforming growth factor-beta (TGF-beta). Serum levels of IL–4, IL–10 and TGF-β were determined in 45 patients with SIRS: 38 patients had SIRS of infectious origin, whereas seven patients had non-infectious SIRS. Twenty healthy subjects were used as controls.Serum levels of IL–4, IL–10 and TGFg were determined by an immunoenzyme assay. A significant increase of IL–4 was observed in these patients at the time of diagnosis and 5 days later. In contrast, serum levels of IL–10 were not increased at the time of diagnosis, but a slight decrease was noted after 5 days. Serum levels of TGF-β were not increased at time of diagnosis, and a slight increase was observed after 5 days. Serum levels of IL–4 were significantly higher in patients with infectious SIRS at the time of diagnosis, whereas no significant difference between infectious and non-infectious SIRS was noted for serum levels of IL–10 and TGF-β at the time of diagnosis and 5 days later.During SIRS, serum levels of IL–4 were significantly increased with a significant correlation between IL–4 and mortality, and only levels of IL–4 were significantly increased in the SIRS caused by infectious stimuli.

scholarly journals Effect of Probiotic Supplementation along with Calorie Restriction on Metabolic Endotoxemia, and Inflammation Markers in Coronary Artery Disease Patients: A Double Blind Placebo Controlled Randomized Clinical Trial

2020 ◽  
Author(s):  
jalal moludi ◽  
Hossein Samadi Kafil ◽  
Pourya Gholizadeh ◽  
Mohammad Alizadeh ◽  
Hamed Jafari Vayghyan
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Lactobacillus Rhamnosus ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Probiotic Supplementation ◽  
Related Factors ◽  
Double Blind ◽  
Artery Disease ◽  
Metabolic Endotoxemia

Abstract Purpose: Alterations in the gut microbiome (dysbiosis) has been associated with increased microbial translocation, leading to chronic inflammation in coronary artery disease (CAD). It has been proposed that modulation of gut microbiota by probiotic might modify metabolic endotoxemia. Therefore, the purpose of this study was to examine the effects of Lactobacillus rhamnosus GG (LGG) on metabolic endotoxemia, and marker of inflammation in CAD participants. Methods: This study was a 12-weeks randomized, double-blind, and intervention on 44 patients with CAD. Patients were randomly allocated to receive either one LGG capsule 1.6 ×109 colony-forming unit (CFU) or the placebo capsules for 12 weeks. In addition, all the participants were also prescribed a calorie-restricted diet. Serum levels of interleukin-1β (IL-1β), Toll-like receptor 4 (TLR4), interleukin-10 (IL-10), and lipopolysaccharide (LPS), were assessed before and after the intervention. Results: A significant decrease in IL1-Beta concentration (-1.88 ± 2.25, vs. 0.56 ± 1.58 mmol/L, P=0.027), and LPS levels (-5.20 ±2.70 vs. 2.96+ 5.27 mg/L, P=0.016), was observed after the probiotic supplementation compared with the placebo. Participants who had ≥2.5 kg weight loss showed significantly improved cardiovascular-related factors, compared to patients with <2.5 kg weight reduction, regardless of the supplement they took.Conclusion: These data provide preliminary evidence that probiotic supplementation has beneficial effects on metabolic endotoxemia, and mega inflammation in participants with CAD.

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