scholarly journals Anti-Gouty Arthritis and Antihyperuricemia Effects of Sunflower (Helianthus annuus) Head Extract in Gouty and Hyperuricemia Animal Models

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Lanzhou Li ◽  
Meiyu Teng ◽  
Yange Liu ◽  
Yidi Qu ◽  
Yuanzhu Zhang ◽  
...  
Keyword(s):  
Helianthus Annuus ◽  
Inflammatory Cytokines ◽  
Gouty Arthritis ◽  
Nitrogen Monoxide ◽  
Serum Levels ◽  
Joint Space ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Acute Gout ◽  
Monocyte Chemoattractant Protein 1

This study was performed to investigate the therapeutic effects and possible mechanisms of sunflower (Helianthus annuus) head extract (SHE) on gout. First, the components of sunflower head powder and SHE were analyzed systematically. SHE, especially SHEB (extracted with 20% ethanol and 80% double-distilled water), strongly suppressed the swelling of the ankles in rats with acute gout induced by monosodium urate (MSU) crystals and reduced the levels of uric acid and xanthine oxidase (XO) in mice with hyperuricemia induced by oteracil potassium and yeast extract powder. Hematoxylin and eosin staining indicated that SHEB reduced inflammation cells and increased the joint space in the ankle compared with the control rats with MSU-induced gout. In the rats with acute gout, among 13 detected inflammatory cytokines, SHEB significantly enhanced the serum levels of interleukin-10 and the monocyte chemoattractant protein 1α. In the mice with hyperuricemia, SHEB reduced the levels of glutathione peroxidase, superoxide dismutase, malondialdehyde, and nitrogen monoxide in liver tissues. The potential therapeutic effects of SHE on gout are probably due to the production of anti-inflammatory cytokines and the suppression of XO activity via the modulation of oxidative stress status.

scholarly journals Zisheng Shenqi Decoction Ameliorates Monosodium Urate-Mediated Gouty Arthritis in Rats via Promotion of Autophagy through the AMPK/mTOR Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jieru Han ◽  
Guangyu Shi ◽  
Wenhao Li ◽  
Shuhui Wang ◽  
Jixiang Bai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Gouty Arthritis ◽  
Nitrogen Monoxide ◽  
Joint Space ◽  
Mtor Signaling ◽  
Receptor Protein ◽  
Related Factor ◽  
Monosodium Urate ◽  
Mtor Signaling Pathway

Gouty arthritis (GA) is an inflammatory disease owing to the accumulation of monosodium urate (MSU) in joints, leading to redness and burning pain. In this study, the effect of Zisheng Shenqi Decoction (ZSD) on a rat model of MSU-induced GA was investigated. ZSD obviously diminished the right paw thickness, the degree of the swelling of the paw, and the infiltration of the inflammatory cell, as well as cartilage erosion, and widened the joint space in MSU-treated rats. Besides, MSU remarkably elevated the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-18; however, ZSD treatment dose dependently lowered these levels and resulted in a significant decrease in articular elastase activity. Also, ZSD administration increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) but declined malondialdehyde (MDA) and nitrogen monoxide (NO) contents. Importantly, western blotting analysis revealed that NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, IL-1β, nuclear factor-E2-related factor 2 (Nrf2) in the cytoplasm, phosphorylated mammalian target of rapamyclin (p-mTOR), and p62 expressions were downregulated, whereas the levels of nuclear Nrf2, phosphorylated AMP-activated protein kinase (p-AMPK), Beclin-1, and LC3II/I were upregulated by ZSD. Immunofluorescence assay indicated that ZSD evidently promoted nuclear translocation of LC3. Taken together, ZSD inhibited inflammation and oxidative stress and facilitated autophagy through the activation of the AMPK pathway and suppression of the mTOR signaling pathway, demonstrating its potential for preventing and curing GA.

scholarly journals Dynamics of Interleukin-10 Levels in Chronic Rhinosinusitis with/without Allergy

2015 ◽  
Vol 7 (3) ◽  
pp. 163
Author(s):  
Abdul Qadar Punagi ◽  
Sutji Pratiwi Rahardjo
Keyword(s):  
Cohort Study ◽  
Chronic Rhinosinusitis ◽  
Inflammatory Cytokines ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Treatment Approach ◽  
Specific Treatment ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Persistent Problem

BACKGROUND: Rhinosinusitis occurs when the lining of the nasal and sinuses gets inflamed, infected or irritated, become swollen, and create extra mucus, the swollen lining may also interfere with drainage of mucus. Chronic rhinosinusitis (CRS) is a more persistent problem that requires a specific treatment approach. Aim of this study was to determine changes in interleukin (IL)-10 as an anti-inflammatory cytokines in allergic and non-allergic CRS at Makassar. METHODS: A prospective cohort study was designed to assess the level of IL-10 for three times during two weeks of therapy. Medication of Cefadroxil 500 mg 2x1, Pseudoephedrine 30 mg 2x1, Terfenadine 40 mg 2x1 and Methylprednisolone 4 mg 3x1, was conducted during two weeks for 13 subjects in allergic CRS group and 12 subjects in non-allergic CRS group. Results were statistically analyzed with student t-test and paired t-test.RESULTS: The changes in levels of IL-10 in allergic CRS group were increased, but not significant (5.293 to 5.769, p=0.058), and in non-allergic CRS group were decreased, but not significant (6.125 to 5.475, p=0.103). CONCLUSION: The serum levels of IL-10 were not significant increased in allergic CRS group and not significant decreased in non-allergic CRS group. KEYWORDS: interleukin-10, chronic rhinosinusitis, allergy, cefadroxil, pseudoephedrine, terfenadine, methylprednisolone

scholarly journals Therapeutic Effects of Nitric Oxide Inhibition during Experimental Fecal Peritonitis: Role of Interleukin-10 and Monocyte Chemoattractant Protein 1

1998 ◽  
Vol 66 (2) ◽  
pp. 650-655 ◽  
Author(s):  
Cory M. Hogaboam ◽  
Matthew L. Steinhauser ◽  
Harold Schock ◽  
Nicholas Lukacs ◽  
Robert M. Strieter ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Interleukin 10 ◽  
Therapeutic Effects ◽  
Fecal Peritonitis ◽  
Monocyte Chemoattractant Protein 1 ◽  
Nitric Oxide Inhibition ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Oxide Inhibition

ABSTRACT This study demonstrates that the therapeutic effect of a nitric oxide inhibitor in a murine model of fecal peritonitis is mediated in part by increased levels of interleukin-10 (IL-10) and monocyte chemoattractant protein 1 (MCP-1). Female CD1 mice were subjected to cecal ligation and puncture (CLP) with a 21-gauge needle and, immediately following surgery, were injected intraperitoneally with saline,N G-nitro-l-arginine methyl ester (l-NAME; 8 mg/kg), orN G-nitro-d-arginine methyl ester (d-NAME; 8 mg/kg). At 96 h after surgery and drug treatment, 20% of mice that received d-NAME had survived whereas 60% of mice that received l-NAME were alive. To elucidate the effect of l-NAME treatment on chemokine and cytokine production during fecal peritonitis, the levels of macrophage inflammatory protein 2 (MIP-2), IL-10, and MCP-1 were measured in peritoneal washings from additional groups of mice 24 h after the CLP surgery. Peritoneal fluids froml-NAME-treated mice contained significantly higher levels of IL-10 and MCP-1 than did those from d-NAME-treated mice. To elucidate the effect of nitric oxide inhibition on potential cellular sources of IL-10 and MCP-1 in the CLP model, cultured alveolar and peritoneal macrophages were activated with bacterial lipopolysaccharide in the presence of l-NAME; these macrophages produced significantly more MCP-1 than did similarly activated macrophages in the presence of d-NAME. In the CLP surgery model, immunoneutralization of IL-10 alone or IL-10 and MCP-1 together with polyclonal antibodies prior to surgery significantly reduced the survival rates in l-NAME-treated groups compared with l-NAME-treated groups that received preimmune serum. Taken together, these data demonstrate that the inhibition of nitric oxide following experimental CLP fecal peritonitis is therapeutic, in part through the modulatory effect of this treatment on the synthesis of IL-10 and MCP-1.

Essential Oils Downregulate Pro-Inflammatory Cytokines and Nitric Oxide-mediated Oxidative Stress in Alloxan-induced Diabetogenic Rats.

2020 ◽  
Vol 20 ◽  
Author(s):  
Muhammad Ejaz ul Haq ◽  
Muhammad Sajid Hamid Akash ◽  
Kanwal Rehman ◽  
Malik Hassan Mahmood
Keyword(s):  
Nitric Oxide ◽  
Essential Oils ◽  
Inflammatory Cytokines ◽  
Diabetic Complications ◽  
Nitrosative Stress ◽  
Serum Levels ◽  
Control Group ◽  
Therapeutic Effects ◽  
Peripheral Tissues ◽  
Pro Inflammatory Cytokines

Introduction: Hyperglycemia is associated with elevated level of reactive nitrogen species (RNS) that leads to nitrosative stress and exacerbates progression of diabetic complications. Method: Present study was aimed to evaluate therapeutic effects of essential oils (EOs) on increased serum level of nitric oxide (NO) in diabetogenic rats. Diabetogenic rats were treated with EOs separately and/or in combination at the dose of 100 mg/kg, orally for one month. Blood sampling was done at 1st, 15th and 30th day of treatment period to investigate the effect of treatment on biomarkers of diabetic complications. Results: In diabetogenic rats, serum levels of NO, malondialdehyde (MDA) and pro-inflammatory cytokines were significantly increased when compared with that of control group. Whereas, diabetogenic rats treated with EOs decreased serum levels of NO, MDA and pro-inflammatory cytokines up to significant extent when compared with that diabetogenic rats treated with standard antidiabetic drug. Moreover, EOs also increased insulin sensitivity in peripheral tissues and insulin secretion from β-cells of pancreatic islets more efficiently when compared with that of diabetogenic rats. Additionally, it was also found that EOs improved lipid profile and normal functions of kidney and liver as compared to that of diabetogenic rats. Conclusion: Findings of this study indicate that EOs may reduce pro-inflammatory cytokine level by modulating the expression of NO. EOs may also ameliorate the nitrosative stress and maintain glucose homeostasis that are major culprits of diabetic complications.

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 OP39 Treatment of ulcerative colitis With AMT-101, a novel oral interleukin-10 immunomodulatory fusion biologic that traffics across the intestinal epithelium

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S039-S040
Author(s):  
R Mrsny ◽  
B Kanwar ◽  
T Mahmood
Keyword(s):  
Ulcerative Colitis ◽  
Side Effects ◽  
Lamina Propria ◽  
Inflammatory Cytokines ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Oral Gavage ◽  
Intestinal Lamina Propria ◽  
Cynomolgus Monkeys ◽  
Pro Inflammatory Cytokines

Abstract Background While different chronic inflammatory diseases can be correlated with distinct pro-inflammatory cytokines, interleukin-10 (IL-10) represents a central anti-inflammatory cytokine capable of modulating many pro-inflammatory signals. Previous clinical efforts to capture the benefit of IL-10 in suppressing the pro-inflammatory state in inflammatory bowel disease (IBD) patients have been limited by dose-limiting systemic side effects. Methods We have designed a chimaera of human IL-10 genetically fused to a non-toxic and poorly immunogenic fragment of the cholix exotoxin, termed AMT-101, that demonstrated rapid receptor-mediated transcytosis in vitro and in vivo and could activate phospho-STAT3 in cells within the lamina propria following luminal administration (data not shown). Mice with oxazolone-induced colitis were dosed by oral gavage with AMT-101 daily for 12 days, at which time colon tissue and serum were examined for hallmarks of inflammation. Enteric-coated capsules were used to deliver either 1 or 5 mg of AMT-101 to the distal ileum of cynomolgus monkeys; serum was collected to examine PK and PD outcomes in this non-inflamed model. Results Histological changes of colonic tissue associated with oxazolone-induced colitis was blocked by the oral gavage of AMT-101. Increases in serum levels of pro-inflammatory cytokines IL-1b, IL-6, and IL-17A were blunted by AMT-101 treatment. Remarkably, endogenous IL-10 increased in this model in an attempt to correct inflammation, but this was also decreased by the delivery of AMT-101. Cynomolgus monkeys dosed orally with AMT-101 capsules showed very low serum levels compared with those observed after IV injection of 0.5 mg/kg AMT-101. Strikingly, serum levels of IL-1 receptor antagonist (IL-1RA) as an anti-inflammatory PD marker were increased to a greater extent following oral capsule dosing compared with IV administration. Conclusion These studies provide strong pre-clinical evidence that AMT-101 can effectively reach the intestinal lamina propria to delivery biologically-active IL-10 following transcytosis across the intestinal epithelium. Importantly, the gut-selective nature of the responses observed suggests AMT-101 may alleviate the previous issues of dose-limiting side effects observed with systemic administration of IL-10 and point to the intestinal lamina propria as a critical site of IL-10’s immunomodulatory actions. AMT-101 has advanced to the clinic and is currently being evaluated in a Phase1b trial in patients with active ulcerative colitis.

scholarly journals Ameliorative Effect of Daidzein on Cisplatin-Induced Nephrotoxicity in Mice via Modulation of Inflammation, Oxidative Stress, and Cell Death

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Hongzhou Meng ◽  
Guanghou Fu ◽  
Jie Shen ◽  
Kezhen Shen ◽  
Zhijie Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Inflammatory Cytokines ◽  
Apoptotic Cell ◽  
Kidney Injury ◽  
Interleukin 10 ◽  
Tunel Staining ◽  
Monocyte Chemoattractant Protein 1 ◽  
Nitrative Stress

Oxidative stress and inflammation are part and parcel of cisplatin-induced nephrotoxicity. The purpose of this work is to study the role of soy isoflavone constituent, daidzein, in cisplatin-induced renal damage. Cisplatin-induced nephrotoxicity was evident by the histological damage in proximal tubular cells and by the increase in serum neutrophil gelatinase-associated lipocalin (NGAL), blood urea nitrogen (BUN), creatinine, and urinary kidney injury molecule-1 (KIM-1). Cisplatin-induced cell death was shown by TUNEL staining and caspase-3/7 activity. Daidzin treatment reduced all kidney injury markers (NGAL, BUN, creatinine, and KIM-1) and attenuated cell death (apoptotic markers). In cisplatin-induced kidney injury, renal oxidative/nitrative stress was manifested by the increase in lipid peroxidation and protein nitration. Cisplatin induced the reactive oxygen species-generating enzyme NOX-2 and impaired antioxidant defense enzyme activities such as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities. Cisplatin-induced oxidative/nitrative stress was attenuated by daidzein treatment. Cisplatin induced CD11b-positive macrophages in kidneys and daidzein attenuated CD11b-positive cells. Daidzein attenuated cisplatin-induced inflammatory cytokines tumor necrosis factorα(TNFα), interleukin 10 (IL-10), interleukin 18 (IL-18), and monocyte chemoattractant protein-1 (MCP-1). Daidzein attenuated cell deathin vitro. Our data suggested that daidzein attenuated cisplatin-induced kidney injury through the downregulation of oxidative/nitrative stress, immune cells, inflammatory cytokines, and apoptotic cell death, thus improving kidney regeneration.

scholarly journals Epidermal green autofluorescence intensity is significantly associated with the serum levels of multiple cytokines of LPS-exposed mice

2019 ◽  
Author(s):  
Yujia Li ◽  
Mingchao Zhang ◽  
Zhaoxia Yang ◽  
Weihai Ying
Keyword(s):  
Serum Levels ◽  
Inflammatory Factors ◽  
Therapeutic Effects ◽  
Health State ◽  
Monocyte Chemoattractant Protein 1 ◽  
Non Invasive ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Highly Correlated ◽  
Stimulating Factor

AbstractInflammation plays various crucial pathological and physiological roles, in which a number of pro-inflammatory and anti-inflammatory cytokines are important mediators. It is of great scientific and clinical significance to search for non-invasive approaches for evaluating cytokine levels in the blood. Our previous study reported that epidermal green autofluorescence (AF) intensity of LPS-exposed mice is highly correlated with LPS doses. In our current study, we determined if epidermal green AF intensity is associated with the serum levels of various cytokines in the LPS-exposed mice. We found that both epidermal green AF intensity and LPS doses are significantly associated with the serum levels of key cytokines including interleukin-1β (IL-1β), IL-6 and IL-10. Both epidermal green AF intensity and LPS doses are also significantly associated with the pro-inflammatory factors including IL-2, IL-12(p40), monocyte chemoattractant protein-1 (MCP-1), MIP-1α, MIP-1β, and regulated on activation, normal T cell expressed and secreted (RANTES/CCL5), as well as anti-inflammatory factors including IL-5 and granulocyte colony stimulating factor (G-CSF). Our findings have suggested that detection of epidermal green AF intensity may become first approach for non-invasive evaluation of certain cytokine levels in human body, which could profoundly enhance our capacity to evaluate inflammation levels for monitoring health state, disease state and therapeutic effects.

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