scholarly journals The Effects of New Zealand Grown Ginseng Fractions on Cytokine Production from Human Monocytic THP-1 Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1158
Author(s):  
Wei Chen ◽  
Prabhu Balan ◽  
David G. Popovich
Keyword(s):  
New Zealand ◽  
Inflammatory Cytokines ◽  
Transforming Growth Factor Beta ◽  
Inflammatory Cytokine ◽  
Transforming Growth Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Pro-inflammatory cytokines and anti-inflammatory cytokines are important mediators that regulate the inflammatory response in inflammation-related diseases. The aim of this study is to evaluate different New Zealand (NZ)-grown ginseng fractions on the productions of pro-inflammatory and anti-inflammatory cytokines in human monocytic THP-1 cells. Four NZ-grown ginseng fractions, including total ginseng extract (TGE), non-ginsenoside fraction extract (NGE), high-polar ginsenoside fraction extract (HPG), and less-polar ginsenoside fraction extract (LPG), were prepared and the ginsenoside compositions of extracts were analyzed by HPLC using 19 ginsenoside reference standards. The THP-1 cells were pre-treated with different concentrations of TGE, NGE, HPG, and LPG, and were then stimulated with lipopolysaccharide (LPS). The levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and anti-inflammatory cytokines, such as interleukin-10 (IL-10), and transforming growth factor beta-1 (TGF-β1), were determined by enzyme-linked immunosorbent assay (ELISA). TGE at 400 µg/mL significantly inhibited LPS-induced TNF-α and IL-6 productions. NGE did not show any effects on inflammatory secretion except inhibited IL-6 production at a high dose. Furthermore, LPG displayed a stronger effect than HPG on inhibiting pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) productions. Particularly, 100 µg/mL LPG not only significantly inhibited the production of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, but also remarkably enhanced the production of anti-inflammatory cytokine IL-10. NZ-grown ginseng exhibited anti-inflammatory effects in vitro, which is mainly attributed to ginsenoside fractions (particularly less-polar ginsenosides) rather than non-saponin fractions.

scholarly journals P0527AROLE OF PROMOTING INFLAMMATION OF KLF6 IN ACUTE KIDNEY INURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Dan Li ◽  
Chenyu Li ◽  
Yan Xu
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Tnf Α ◽  
Public Dataset ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background and Aims Acute kidney injury (AKI), commonly appeared in cardiac arrest, surgery and kidney transplantation which involved in ischemia-reperfusion (IR) injury of kidney. However, the mechanisms underlying inflammatory response in IR AKI is still unclear. Method Public dataset showed kruppel-like factor 6 (KLF6) was significantly highly expressed (P<0.05) in AKI, implies KLF6 might be associated with AKI. To evaluate the mechanism of KLF6 on IR AKI, 30 rats were randomly divided into sham and IR group, and were sacrificed at 0 h, 3 h, 6 h, 12 h or 24 h after IR. Results The results showed KLF6 expression was peaking at 6 h after IR, and the expression of pro-inflammatory cytokines MCP-1 and TNF-α were increased both in serum and kidney tissues after IR, while anti-inflammatory cytokine IL-10 was decreased after IR. Furthermore, in vitro results showed KLF6 knock-down reduced the pro-inflammatory cytokines expression and increased the anti-inflammatory cytokines expression. Conclusion These results suggest that (1) KLF6 might be a novel biomarker for early diagnosis of AKI and (2) targeting KLF6 expression may offer novel strategies to protect kidneys from IR AKI Figure KLF6, AKI, Control Inflammation

Abstract 088: Chronic Efferent Vagal Stimulation Enhances Norepinephrine-mediated Inhibition of Splenic Pro-inflammatory Cytokine Release in Lupus Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Grace S Pham ◽  
Amber S Fairley ◽  
Keisa W Mathis
Keyword(s):  
Inflammatory Cytokines ◽  
Lupus Erythematosus ◽  
Inflammatory Cytokine ◽  
Vagal Stimulation ◽  
Reproductive Age ◽  
Cytokine Release ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Stimulation Of ◽  
Pro Inflammatory Cytokines

Hypertension is prevalent in the autoimmune disease systemic lupus erythematosus (SLE), occurring with alarming frequency in reproductive-age women. Recent studies implicate the adaptive immune system in the development and maintenance of hypertension, and neuroimmune pathways may regulate this source of inflammation. One example is the cholinergic anti-inflammatory pathway (CAP), an endogenous nerve-to-spleen mechanism that regulates splenic pro-inflammatory cytokine release. We hypothesized that this pathway is impaired in SLE and that chronic stimulation of the CAP at the level of the efferent vagus nerve would attenuate hypertension in SLE. Starting at 30 and 32 weeks of age, female NZBWF1 SLE mice and NZW control mice were treated with the pharmacologic efferent vagal stimulators CNI-1493 (CNI; 8mg/kg; twice weekly; i.p.) or galantamine (GAL; 4mg/kg; daily; i.p.), or saline. At 34 weeks of age, we measured mean arterial pressure (MAP), finding that MAP (mmHg) in SLE mice was elevated compared to controls (139.83 ± 4.56 vs. 120.70 ± 2.96; n=4-6/group, p = 0.002), while the rise in MAP was prevented by CNI (134.45 ± 3.07)and GAL (129.25 ± 3.97) in SLE mice. We further hypothesized that splenocytes isolated from SLE mice conditioned by efferent vagal stimulation would release fewer pro-inflammatory cytokines in the presence of norepinephrine, which stimulates splenic β2 adrenergic receptors. We incubated isolated splenocytes for 24 hours at 37°C with and without norepinephrine (100 μM), then measured pro-inflammatory cytokines in the supernatant via ELISA. Compared to control mice, splenocytes from SLE mice secreted 70.7% and 146.5% higher concentrations of IL-6 and TNF-α (8.24 vs. 4.83 and 2.79 vs. 1.13 pg/mL, respectively; n=2/group) in the presence of norepinephrine. Compared to saline-treated SLE mice, splenocytes from CNI and GAL-treated SLE mice released fewer cytokines when incubated with norepinephrine (8.24 vs. 5.31 and 5.79 pg/mL IL-6; 2.79 vs. 2.18 and 0.81 pg/mL TNF-α; n=2/group). These in vivo and in vitro data suggest that stimulation of the CAP at the level of the efferent vagus may promote anti-inflammatory splenocyte activity, which may be protective against hypertension in the setting of chronic inflammation.

scholarly journals Electroacupuncture Improves M2 Microglia Polarization and Glia Anti-inflammation of Hippocampus in Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Lushuang Xie ◽  
Yi Liu ◽  
Ning Zhang ◽  
Chenyu Li ◽  
Aaron F. Sandhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Tnf Α ◽  
Microglia Polarization ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Background: Alzheimer’s disease (AD) is a neurodegenerative disease characterized by loss of recognition and memory. Neuroinflammation plays pivotal roles in the pathology of AD and affects the progression of the disease. Astrocyte and microglia, as main immune executors in the central nervous system (CNS), participate into the inflammatory response in AD. Glia polarize into different phenotypes during neurodegeneration. Pro-inflammatory glia produce cytokines (IL-1β, TNF-α, and IL-6) resulting into debris aggregates and neurotoxicity. Anti-inflammatory phenotypes produce cytokines (IL-4 and IL-10) to release the inflammation. Electroacupuncture is a useful treatment that has been found to slow the neurodegeneration in animals through experimentation and in humans through clinical trials. The aim of this study was to uncover the mechanisms of glia activation, microglia polarization, and cytokine secretion regulated by electroacupuncture as a treatment for AD.Methods: Twenty male Sprague–Dawley (SD) rats were randomly divided into four groups: Control group (Control), Normal saline group (NS), AD group (AD), and Electroacupuncture group (Acupuncture). The AD and Acupuncture groups were bilaterally injected with Aβ1–42 into the CA1 field of the hippocampus. The Acupuncture group received electroacupuncture stimulation on the acupoint “Baihui” (GV20) for 6 days per week for a total of 3 weeks. The Morris Water Maze (MWM) was used to evaluate learning and memory capacity. Immunofluorescence was used to stain GFAP and Iba1 of the DG and CA1 in the hippocampus, which, respectively, expressed the activation of astrocyte and microglia. The M1 microglia marker, inducible nitric oxide synthase (iNOS), and M2 marker Arginase 1 (Arg1) were used to analyze the polarization of microglia. The pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), anti-inflammatory cytokines (IL-4 and IL-10), and pathway-molecules (p65 and Stat6) were tested to analyze the glia inflammatory response by immunofluorescence and polymerase chain reaction (PCR).Results: The MWM results showed that electroacupuncture improves the escape latency time and the swimming distance of AD rats. The number of GFAP and Iba1 cells significantly increased in AD rats, but electroacupuncture decreased the cells. The iNOS-positive cells were significantly increased in AD, and electroacupuncture decreased the positive cells. Electroacupuncture elevated Arg1-positive cells in AD rats. Electroacupuncture decreased the glia pro-inflammatory cytokine expression and increased the anti-inflammatory cytokine expression in AD rats. Furthermore, electroacupuncture inhibited the NF-κB pathway molecule (p65) while raising the Stat6 pathway molecule (Stat6).Conclusion: These results provide evidence that electroacupuncture improves the recognition abilities and memory of AD rats. Electroacupuncture inhibits the activation of glia and polarizes microglia toward the M2 phenotype. Electroacupuncture decreased the pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) and increased the anti-inflammatory cytokines (IL-4 and IL-10). Furthermore, electroacupuncture affects the immune responses through inhibition of NF-κB pathway but activation of Stat6 pathway.

scholarly journals The pattern of pro- and anti-inflammatory cytokine secretion in patients with secondary edematous breast cancer

2021 ◽  
Vol 23 (4) ◽  
pp. 536-540
Author(s):  
O. M. Bilyi ◽  
N. A. Mitriaieva ◽  
M. V. Krasnoselskyi ◽  
L. V. Hrebinyk
Keyword(s):  
Breast Cancer ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Serum Levels ◽  
Special Treatment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Secondary edematous breast cancer (SEBC), T4b, has a poor prognosis. The aim of this study is to examine the balance in serum levels of pro-inflammatory (TNFά, IL-8) and anti-inflammatory (IL-4) cytokines in patients with SEBC before special treatment. Materials and methods. A total of 87 patients with breast cancer (BC) were examined before treatment: 42 patients with SEBC in T4bN0-3M0 stage and 45 BC patients in T3-4N1-3M0 stage without edema. The control group consisted of 15 patients with fibroadenomas. The serum levels of cytokines (IL-4, IL-8, TNFά) in the patients was determined using the enzyme-linked immunosorbent assay. Results. In the SEBC patients as compared to the patients without cancer, the serum pro-inflammatory cytokine (IL-8, TNFά) levels were significantly increased and the anti-inflammatory cytokine (IL-4) level was slightly increased in 22 %. In BC without edema, an imbalance was noted in favor of pro-inflammatory cytokines, but in SEBC it was more pronounced (31.6 versus 12.4 and 5.6 versus 3.2, respectively). Conclusions. In the majority of SEBC patients, there is an imbalance in the cytokine profile in favor of the pro-inflammatory cytokines (IL-8, TNFά). SEBC patients with elevated levels of both pro- and anti-inflammatory cytokines before treatment are the highest risk group of tumor progression and metastasis. Inhibition of the IL-8 effects or related CXC chemokines, TNFά, and others may have important consequences for the systemic treatment of SEBC.

Pro- and anti-inflammatory response profile modulates Plasmodium falciparum malaria outcomes among subjects from Baiyeku, Ikorodu, Lagos, Nigeria.

2020 ◽  
Author(s):  
Daniel Osegi Okpokor ◽  
Olusola Ajibaye ◽  
Peter Mac Asaga ◽  
Ikechukwu Nwankwo ◽  
Anthony Danaan Dakul
Keyword(s):  
Plasmodium Falciparum ◽  
Inflammatory Cytokines ◽  
Parasite Density ◽  
World Health ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Significant Difference ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Background Available evidence indicates that the various stages of the malaria parasite life cycle elicit specific immune responses of which the relative levels of pro-inflammatory cytokines are key to disease progression, killing the parasite and mediating disease outcomes. This study will inform immunological interventions against malaria and thus malaria vaccine developments programs/efforts. Methods A total of four hundred and sixty-two participants were screened in a community survey for Plasmodium falciparum (P. falciparum) malaria in Baiyeku, Lagos, Nigeria. P. falciparum parasitaemia was determined by Microscopy using thick and thin blood films stained by Giemsa method using World Health Organization parasitology laboratory protocol whist the serum levels of IL-10, IFNγ and TNFα were determined by Enzyme linked immunosorbent assay [ELISA]. Data analysis was done by One-way Analysis of Variance (ANOVA), Chi square (X²) and Student’s T-test in statistical package for the social sciences (SPSS) version 24 was used to test statistical significance between the symptomatic groups and asymptomatic in relation to age, gender and BMI of the participants.Results A total of 70 (15.2 %) participants were microscopically positive for P. falciparum of which 70% were female, 30% were males while children aged 1-17 years were 65.7%. The geometric mean parasite density (GMPD) was significantly (p=0.001) higher among females than males. The GMPD of participants < 5 years was also significantly (p=0.001) higher than other age groups. About 46.8% of the participants were underweight (BMI < 18.5) also had the highest parasite intensity. The TNFα, IFNγ and IL-10 levels were significantly (p 0.05) higher in the infected than the uninfected participants. IFN-γ values were significantly (p=0.014) elevated among the symptomatic than the asymptomatic participants while there was no significant difference (P>0.053) in the levels of TNF-α and IL-10 (P>0.093) between the symptomatic and asymptomatic participants. Notably, the IL-10 levels were the most elevated amongst the participants with the highest parasite density.Conclusion The prevalence of P. falciparum obtained in this study area which is endemic for malaria is 15.2% suggesting a significant reduction of the disease over time. The awareness of the disease which is now more than before seems to contribute to the lowering of prevalence of the disease in the community. There was a positive relationship between TNF-alpha levels and body temperature. However, compared with the anti-inflammatory cytokine (IL-10) in this study, the levels of the pro-inflammatory cytokines (IFN-γ and TNF-α) were lower due to the negative action of the anti-inflammatory cytokines. IL-10 value increased as parasitemia increased (p=0.073). These findings suggest that higher levels of anti-inflammatory cytokines, especially IL-10 levels may contribute to pathogenesis of uncomplicated malaria.

scholarly journals Dental Follicle Stem Cells Ameliorate Lipopolysaccharide-Induced Inflammation by Secreting TGF-β3 and TSP-1 to Elicit Macrophage M2 Polarization

2018 ◽  
Vol 51 (5) ◽  
pp. 2290-2308 ◽  
Author(s):  
Xiaochuan Chen ◽  
Bo Yang ◽  
Jun Tian ◽  
Hong Hong ◽  
Yu Du ◽  
...  
Keyword(s):  
Stem Cells ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Paracrine Factors ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Follicle Stem Cells ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Background/Aims: Increasing evidence has demonstrated the novel roles of mesenchymal stem cells (MSCs) in immunotherapy. However, difficulty in acquiring these cells and possible ethical issues limited their application. Recently, we have isolated a unique MSC population from dental follicles with potent stem cell-like properties. This study focused on the effects of dental follicle stem cells (DFSCs) on macrophage activation and polarization to determine their role in immunomodulation and to test if DFSCs are a promising cell source for MSC-based immunotherapy. Methods: Rat acute lung injury (ALI) models induced by Lipopolysaccharide (LPS) were applied to test the immune-modulatory effects of DFSC/DFSC-CM in vivo. The pulmonary permeability was determined by the dry / wet weight ratios of the left upper lung lobe. The lung histopathological damage was graded on a 0 to 4+ scale. And the inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were tested by ELISA. Then we established LPS-induced inflamed macrophage models in vitro. Inflammatory cytokine production and polarization marker expression were measured by RT-qPCR, ELISA, western blot and flow cytometric analysis in macrophages following DFSC-CM treatment. The paracrine factors in DFSC-CM were revealed by a RayBiotech Protein Array. Thereafter, neutralization studies were performed to confirm the potential immune regulators in DFSC-CM. Results: The DFSC/DFSC-CM not only attenuated histopathological damage and pulmonary permeability, but also downregulated pro-inflammatory cytokines MCP-1, IL-1, IL-6 and TNF-α, and upregulated anti-inflammatory cytokine IL-10 in BALF. Immunofluorescence staining revealed the increased expression of macrophage M2 marker Arg-1. Further in vitro study revealed that macrophages switched to an anti-inflammatory M2 phenotype when co-cultured with DFSC-CM, characterized by suppressed production of pro-inflammatory cytokines MCP-1, IL-1, IL-6, TNF-α and M1-polarizing markers iNOS and CD86; and increased expression of the anti-inflammatory cytokine IL-10 and the M2-polarizing markers Arg-1 and CD163. A RayBiotech Protein Array revealed 42 differentially expressed (> 2-fold) paracrine factors in DFSC-CM compared with the serum-free Ham’s F-12K medium, among which TGF-β3 and Thrombospondin-1 (TSP-1) were upregulated by 18- and 105-fold, respectively. Neutralization studies confirmed the immunoregulatory roles of TGF-β3 and TSP-1 in macrophage activation and polarization. Conclusion: These results indicated that DFSCs can reprogram macrophages into the anti-inflammatory M2 phenotype, the paracrine factors TGF-β3 and TSP-1 may be one of the underlying mechanisms. This study supports the hypothesis that DFSCs are promising for MSC-based immunotherapy.

scholarly journals Phytochemical Constituents of Citrus hystrix DC. Leaves Attenuate Inflammation via NF-κB Signaling and NLRP3 Inflammasome Activity in Macrophages

Biomolecules ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 105
Author(s):  
Watunyoo Buakaew ◽  
Rungnapa Pankla Sranujit ◽  
Chanai Noysang ◽  
Yordhathai Thongsri ◽  
Pachuen Potup ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Ethanolic Extract ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Cancer ◽  
Polymerase Chain ◽  
Anti Inflammatory ◽  
Immunoblotting Technique ◽  
Pro Inflammatory Cytokines

Citrus hystrix DC. (CH) is found in many countries in Southeast Asia. This plant has been reported for anti-microbial, anti-cancer and anti-inflammatory bioactivities. However, the anti-inflammatory and anti-inflammasome properties of the leaves remain poorly understood. This study aimed to investigate the effect of CH leaves on NLRP3 and NF-κB signaling pathways. CH leaves were sequentially extracted using hexane, ethyl acetate and 95% ethanol to give three crude extracts. An active compound, lupeol was fractionated from the ethanolic extract using chromatographic techniques, and its structure was identified and confirmed by spectroscopic methods. Anti-inflammatory activities were observed on both lipopolysaccharide-stimulated and NLRP3 adenosine triphosphate-induced macrophages. The release of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) was analyzed by Enzyme-Linked Immunosorbent Assay (ELISA). Real-time qRT-polymerase chain reaction (PCR) was used to measure inflammatory-associated gene expression. NF-κB protein expressions were investigated using the immunoblotting technique. The active fraction of ethanolic CH leaves and lupeol significantly reduced the release of pro-inflammatory cytokines and suppressed the expression of both inflammasome genes and NF-κB proteins. The ethanolic extract of CH leaves and lupeol showed potent anti-inflammatory activities by targeting NF-κB and NLRP3 signaling pathways.

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

scholarly journals Inflammatory cytokines-stimulated human muscle stem cells ameliorate ulcerative colitis via the IDO-TSG6 axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shengchao Zhang ◽  
Jiankai Fang ◽  
Zhanhong Liu ◽  
Pengbo Hou ◽  
Lijuan Cao ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Human Muscle ◽  
Enzyme Linked Immunosorbent Assay ◽  
Muscle Stem Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

Abstract Background Muscle stem cells (MuSCs) are absolutely required for the formation, repair, and regeneration of skeletal muscle tissue. Increasing evidence demonstrated that tissue stem cells, especially mesenchymal stem cells (MSCs), can exert therapeutic effects on various degenerative and inflammatory disorders based on their immunoregulatory properties. Human mesenchymal stem cells (hMSCs) treated with interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were reported to possess anti-inflammatory functions by producing TNF-stimulated gene 6 (TSG-6). However, whether human muscle stem cells (hMuSCs) also possess TSG-6 mediated anti-inflammatory functions has not been explored. Methods The ulcerative colitis mouse model was established by subjecting mice to dextran sulfate sodium (DSS) in drinking water for 7 days. hMuSCs were pretreated with IFN-γ and TNF-α for 48 h and were then transplanted intravenously at day 2 of DSS administration. Body weights were monitored daily. Indoleamine 2,3-dioxygenase (IDO) and TSG-6 in hMuSCs were knocked down with short hairpin RNA (shRNA) and small interfering RNA (siRNA), respectively. Colon tissues were collected for length measurement and histopathological examination. The serum level of IL-6 in mice was measured by enzyme-linked immunosorbent assay (ELISA). Real-time PCR and Western blot analysis were performed to evaluate gene expression. Results hMuSCs treated with inflammatory factors significantly ameliorated inflammatory bowel disease (IBD) symptoms. IDO and TSG-6 were greatly upregulated and required for the beneficial effects of hMuSCs on IBD. Mechanistically, the tryptophan metabolites, kynurenine (KYN) or kynurenic acid (KYNA) produced by IDO, augmented the expression of TSG-6 through activating their common receptor aryl hydrocarbon receptor (AHR). Conclusion Inflammatory cytokines-treated hMuSCs can alleviate DSS-induced colitis through IDO-mediated TSG-6 production.

The anti-inflammatory and anti-fibrotic effects of tadalafil in thioacetamide-induced liver fibrosis in rats

2018 ◽  
Vol 96 (12) ◽  
pp. 1308-1317 ◽  
Author(s):  
Heba M. Mansour ◽  
Abeer A.A. Salama ◽  
Rania M. Abdel-Salam ◽  
Naglaa A. Ahmed ◽  
Noha N. Yassen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Inflammatory Cytokines ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Interleukin 1 ◽  
Health Concern ◽  
Dependent Manner ◽  
Serum Transaminases ◽  
Anti Inflammatory

Liver fibrosis is a health concern that leads to organ failure mediated via production of inflammatory cytokines and fibrotic biomarkers. This study aimed to explore the protective effect of tadalafil, a phosphodiesterase-5 inhibitor, against thioacetamide (TAA)-induced liver fibrosis. Fibrosis was induced by administration of TAA (200 mg/kg, i.p.) twice weekly for 6 weeks. Serum transaminases activities, liver inflammatory cytokines, fibrotic biomarkers, and liver histopathology were assessed. TAA induced marked histopathological changes in liver tissues coupled with elevations in serum transaminases activities. Furthermore, hepatic content of nitric oxide and tumor necrosis factor-alpha, interleukin-6, and interleukin-1 beta were elevated, together with a reduction of interleukin-10 in the liver. In addition, TAA increased hepatic contents of transforming growth factor-beta, hydroxyproline, alpha-smooth muscle actin, and gene expression of collagen-1. Pretreatment with tadalafil protected against TAA-induced liver fibrosis, in a dose-dependent manner, as proved by the alleviation of inflammatory and fibrotic biomarkers. The effects of tadalafil were comparable with that of silymarin, a natural antioxidant, and could be assigned to its anti-inflammatory and anti-fibrotic properties.

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