Bifidobacterium infantis has a beneficial effect on 5-fluorouracil-induced intestinal mucositis in rats

2015 ◽  
Vol 6 (1) ◽  
pp. 113-118 ◽  
Author(s):  
K.-T. Yuan ◽  
H.-L. Yu ◽  
W.-D. Feng ◽  
P. Chong ◽  
T. Yang ◽  
...  
Keyword(s):  
Body Weight ◽  
Interleukin 1 ◽  
Nuclear Antigen ◽  
Inflammatory Factors ◽  
High Dose ◽  
Villus Height ◽  
Bifidobacterium Infantis ◽  
Toxic Side Effect ◽  
Necrosis Factor Alpha ◽  
Intestinal Mucositis

Intestinal mucositis is a common toxic side effect in cancer patients receiving high-dose chemotherapy. This study aimed to evaluate the beneficial effects of Bifidobacterium infantis in a rat model of intestinal mucositis induced by 5-fluorouracil (5-FU). Thirty male Sprague-Dawley rats were divided into three groups: control, 5-FU, and 5-FU + B. infantis. A single intraperitoneal injection of 5-FU (150 mg/kg) was used to induce intestinal mucositis. B. infantis (1×109 cfu) was administered for 11 days, starting from 7 days before 5-FU injection. Intestinal mucositis was evaluated based on body weight, villus height, immunohistological expression of proliferating cell nuclear antigen (PCNA) and nuclear factor kappa beta (NF-κB), levels of the pro-inflammatory factors interleukin 1 beta and tumour necrosis factor alpha, and myeloperoxidase (MPO) concentration. The results showed that the 5-FU + B. infantis group demonstrated a higher body weight and villus height, increased expression of PCNA, reduced expression of NF-κB and pro-inflammatory factors, and lower MPO concentration compared to the 5-FU group. These data suggest that probiotic B. infantis is effective in reducing chemotherapy-induced intestinal mucositis in rats.

scholarly journals Possible Protective Effect of Diacerein on Doxorubicin-Induced Nephrotoxicity in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Marwa M. M. Refaie ◽  
Entesar F. Amin ◽  
Nashwa F. El-Tahawy ◽  
Aly M. Abdelrahman
Keyword(s):  
Protective Effect ◽  
Low Dose ◽  
Caspase 3 ◽  
Interleukin 1 ◽  
Treated Group ◽  
Limiting Factors ◽  
High Dose ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Nephrotoxicity is one of the limiting factors for using doxorubicin (DOX). Interleukin 1 has major role in DOX-induced nephrotoxicity, so we investigated the effect of interleukin 1 receptor antagonist diacerein (DIA) on DOX-induced nephrotoxicity. DIA (25 and 50 mg/kg/day) was administered orally to rats for 15 days, in the presence or absence of nephrotoxicity induced by a single intraperitoneal injection of DOX (15 mg/kg) at the 11th day. We measured levels of serum urea, creatinine, renal reduced glutathione (GSH), malondialdehyde (MDA), total nitrites (NOx), catalase, and superoxide dismutase (SOD). In addition, caspase-3, tumor necrosis factor alpha (TNFα), nuclear factor kappa B (NFκB) expressions, and renal histopathology were assessed. Our results showed that DOX-induced nephrotoxicity was ameliorated or reduced by both doses of DIA, but diacerein high dose (DHD) showed more improvement than diacerein low dose (DLD). This protective effect was manifested by significant improvement in all measured parameters compared to DOX treated group by using DHD. DLD showed significant improvement of creatinine, MDA, NOx, GSH, histopathology, and immunohistochemical parameters compared to DOX treated group.

scholarly journals Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 106 ◽  
Author(s):  
Yuanjun Deng ◽  
Kairui Tang ◽  
Runsen Chen ◽  
Yajie Liu ◽  
Huan Nie ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Low Dose ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Model Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

scholarly journals A Randomized Control Trial Study to Determine the Effect of Melatonin on Serum Levels of IL-1β and TNF-α in Patients with Multiple Sclerosis

2020 ◽  
Author(s):  
Masoomeh Yosefifard ◽  
Gholamhassan Vaezi ◽  
Ali Akbar Malekirad ◽  
Fardin Faraji ◽  
Vida Hojati
Keyword(s):  
Multiple Sclerosis ◽  
Interleukin 1 ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Treatment Groups ◽  
Tnf Α ◽  
Significant Difference ◽  
The Central Nervous System

Multiple sclerosis (MS) is the most common neurological disease that happens at a young age. MS is an inflammatory disease; associated with the demyelination of the central nervous system. Therefore, some inflammatory factors are effective in the mechanism and progression of the disease. Melatonin, as a multi-effect substance including anti-inflammatory effects, can reduce symptoms of MS in patients with a change in their inflammatory factors level. In this study, 50 MS patients who were referred to the MS Society of Markazi Province were randomly selected. All patients were treated with routine MS treatment (interferon) and were divided into control (25 placebo recipients) and treatment (25 recipients of 3 mg melatonin per day for 24 weeks) groups. Anthropometric data of patients including height, weight, and age were determined. Blood samples were collected after fasting in order to determine serum levels of interleukin 1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Then, samples were immediately centrifuged for serum separation and sera were transferred to a freezer at -80°C and serum levels of these factors were determined; using ELISA kit. The results of this study showed that there was no significant difference between the control and treatment groups in terms of serum levels of TNF-α. However, the level of IL-1β was significantly reduced in the treatment group compared to the control group, indicating that melatonin decreases this inflammatory substance. Our findings suggest a valuable strategy in the treatment of patients who suffer from MS

scholarly journals Cytokine Kinetics and Other Host Factors in Response to Pneumococcal Pulmonary Infection in Mice

1998 ◽  
Vol 66 (3) ◽  
pp. 912-922 ◽  
Author(s):  
Yves Bergeron ◽  
Nathalie Ouellet ◽  
Anne-Marie Deslauriers ◽  
Marie Simard ◽  
Martin Olivier ◽  
...  
Keyword(s):  
Body Weight ◽  
Bacterial Growth ◽  
Interleukin 1 ◽  
Body Weight Loss ◽  
Lung Weight ◽  
Necrosis Factor Alpha ◽  
Type Ii Pneumocytes ◽  
Growth Loss ◽  
Cd1 Mice ◽  
Factor Alpha

ABSTRACT There is a need for more insight into the pathogenesis ofStreptococcus pneumoniae pneumonia, as the fatality rate associated with this disease remains high despite appropriate antibiotherapy. The host response to pneumococci was investigated after intranasal inoculation of CD1 mice with 107 log-phase CFU of bacteria. We identified five major pathogenesis steps from initial infection to death. In step 1 (0 to 4 h), there was ineffective phagocytosis by alveolar macrophages, with concurrent release of tumor necrosis factor alpha (TNF), interleukin-6 (IL-6), and nitric oxide (NO) in bronchoalveolar lavage (BAL) fluid, TNF, IL-6, and interleukin-1 alpha (IL-1) in lung tissues, and IL-6 in serum, which were associated with tachypnea and hemoconcentration. In step 2 (4 to 24 h), bacterial growth in alveoli and polymorphonuclear cell recruitment from bloodstream to lung tissue (high myeloperoxidase levels) to alveoli were associated with high release of all three cytokines and leukotriene B4(LTB4) in tissue and BAL fluid, as well as transient spillover of IL-1 in serum. In step 3 (24 to 48 h), despite downregulation of TNF and IL-1 in BAL fluid and lungs, there was appearance of injury to alveolar ultrastructure, edema to interstitium, and increase in lung weight as well as regeneration of type II pneumocytes and increased secretion of surfactant; bacteria progressed from alveoli to tissue to blood, and body weight loss occurred. In step 4 (48 to 72 h), strong monocyte recruitment from blood to alveoli was associated with high NO release in tissue and BAL fluid, but there was also noticeable lymphocyte recruitment and leukopenia; bacteremia was associated with TNF and IL-6 release in blood and thrombocytopenia. In step 5 (72 to 96 h), severe airspace disorganization, lipid peroxidation (high malondialdehyde release in BAL fluid), and diffuse tissue damage coincided with high NO levels; there was further increase in lung weight and bacterial growth, loss in body weight, and high mortality rate. Delineation of the sequential steps that contribute to the pathogenesis of pneumococcal pneumonia may generate markers of evolution of disease and lead to better targeted intervention.

scholarly journals The Effect of Scaling and Root Planning on Salivary TNF-α and IL-1α Concentrations in Patients with Chronic Periodontitis

2017 ◽  
Vol 11 (1) ◽  
pp. 573-580 ◽  
Author(s):  
Masoome Eivazi ◽  
Negar Falahi ◽  
Nastaran Eivazi ◽  
Mohammad Ali Eivazi ◽  
Asad Vaisi Raygani ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Interleukin 1 ◽  
Negative Relationship ◽  
Inflammatory Factors ◽  
Control Group ◽  
Pocket Depth ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Root Planning ◽  
Scaling And Root Planning

Objective:Periodontitis is one of the main diseases in the oral cavity that causes tooth loss. The host immune response and inflammatory factors have important role in periodontal tissue. The current study was done with the objective to determine the effect of scaling and root planning on the salivary concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1-alpha (IL-1α).Methods:In this quasi-experimental clinical trial, 29 patients with chronic periodontitis and 29 healthy subjects without periodontitis were studied. Clinical examination findings and salivary TNF-α and IL-1α (using ELISA method) were compared before and after scaling, root planning.Results:Before starting treatment, salivary TNF-α and IL-1α concentrations were higher in healthy control group than in periodontitis group (P< 0.05). Non-surgical treatment increased the concentration of these two biomarkers in the saliva. However, increase in IL-1α concentration was not statistically significant (P= 0.056). There was a negative relationship between TNF-α and IL-1α levels with pocket depth and attachment loss (P< 0.05).Conclusion:Scaling and root planning improved periodontal disease indices and salivary TNF-α and IL-1α levels.

scholarly journals Discovery of Active Ingredients Targeted TREM2 by SPR Biosensor-UPLC/MS Recognition System, and Investigating the Mechanism of Anti-Neuroinflammatory Activity on the Lignin-Amides from Datura metel Seeds

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5946
Author(s):  
Si-Yi Wang ◽  
Yan Liu ◽  
Xiao-Mao Li ◽  
Adnan Mohammed Algradi ◽  
Hai Jiang ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Interleukin 1 ◽  
Recognition System ◽  
Inflammatory Factors ◽  
Active Ingredients ◽  
Necrosis Factor Alpha ◽  
Pyrin Domain ◽  
Spr Biosensor ◽  
Datura Metel ◽  
Bv2 Microglia

As a new target protein for Alzheimer’s disease (AD), the triggering receptor expressed on myeloid Cells 2 (TREM2) was expressed on the surface of microglia, which was shown to regulate neuroinflammation, be associated with a variety of neuropathologic, and regarded as a potential indicator for monitoring AD. In this study, a novel recognition system based on surface plasmon resonance (SPR) for the TREM2 target spot was established coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-MS), in order to screen the active ingredients targeting TREM2 from Datura metel seeds. The results showed that four lignan-amides were discovered as candidate compounds by SPR biosensor-UPLC/MS recognition analysis. According to the guidance of the active ingredients discovered by the system, the lignin-amides from Datura metel seeds (LDS) were preliminarily identified as containing 27 lignan-amides, which were enriched compositions by the HP-20 of Datura metel seeds. Meanwhile, the anti-inflammatory activity of LDS was evaluated in BV2 microglia induced by LPS. Our experimental results demonstrated that LDS could reduce NO release in LPS-treated BV2 microglia cells and significantly reduce the expression of the proteins of inducible Nitric Oxide Synthase (iNOS), cyclooxygenase 2 (COX-2), microtubule-associated protein tau (Tau), and ionized calcium-binding adapter molecule 1 (IBA-1). Accordingly, LDS might increase the expression of TREM2/DNAX-activating protein of 12 kDa (DAP12) and suppress the Toll-like receptor SX4 (TLR4) pathway and Recombinant NLR Family, Pyrin Domain Containing Protein 3 (NLRP3)/cysteinyl aspartate specific proteinase-1 (Caspase-1) inflammasome expression by LDS in LPS-induced BV2 microglial cells. Then, the inhibitory release of inflammatory factors Interleukin 1 beta (IL-1β), Interleukin 6 (IL-6), and Tumor necrosis factor-alpha (TNFα) inflammatory cytokines were detected to inhibit neuroinflammatory responses. The present results propose that LDS has potential as an anti-neuroinflammatory agent against microglia-mediated neuroinflammatory disorders.

scholarly journals Immunohistochemical Analysis of Intestinal and Central Nervous System Morphology in an Obese Animal Model (Danio rerio) Treated with 3,5-T2: A Possible Farm Management Practice?

Animals ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1131
Author(s):  
Roberta Imperatore ◽  
Lea Tunisi ◽  
Isabella Mavaro ◽  
Livia D’Angelo ◽  
Chiara Attanasio ◽  
...  
Keyword(s):  
Body Weight ◽  
Danio Rerio ◽  
Management Practice ◽  
Serum Triglyceride ◽  
Immunohistochemical Analysis ◽  
The Body ◽  
Brain Inflammation ◽  
Nuclear Antigen ◽  
Inflammatory Factors ◽  
Fish Intestine

The 3,5-diiodo-L-thyronine (3,5-T2) is an endogenous metabolite of thyroid hormones, whose administration to rodents fed high-fat diet (HFD) prevents body weight increase and reverts the expression pattern of pro-inflammatory factors associated to HFD. The diet-induced obese (D.I.O.) zebrafish (Danio rerio) has been recently used as an experimental model to investigate fundamental processes underlying central and peripheral obesity-driven inflammation. Herein, we aim to understand the role of 3,5-T2 in regulating central and peripheral inflammation in D.I.O. model of zebrafish. 3,5-T2 (10 nM and 100 nM) was administered with the obesity-inducing diet (D.I.O. with 3,5-T2) or after 4 weeks of obesity-inducing diet (D.I.O. flw 3,5-T2). 3,5-T2 significantly increased the body weight and serum triglyceride levels in D.I.O. zebrafish in both conditions. Moreover, 3,5-T2 sustained or increased inflammation in the anterior (AI) and mid (MI) intestine when administered with the obesity-inducing diet, as indicated by the immunoexpression of the inflammatory markers tumor-necrosis factor-α (TNFα), cyclooxygenase 2 (COX2), calnexin, caspase 3, and proliferating cell nuclear antigen (PCNA). On the contrary, when 3,5-T2 was administered after the obesity-inducing diet, partly reverted the intestinal alteration induced by D.I.O. In addition, brain inflammation, as indicated by the increase in the activation of microglia, was detected in D.I.O. zebrafish and D.I.O. treated with 3,5-T2. These findings reveal that the effects of 3,5-T2 on fish intestine and brain can deviate from those shown in obese mammals, opening new avenues to the investigation of the potential impact of this thyroid metabolite in different diseases including obesity.

scholarly journals Serum Inflammatory Factor Profiles in the Pathogenesis of High-Altitude Polycythemia and Mechanisms of Acclimation to High Altitudes

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Hai Yi ◽  
Qianjin Yu ◽  
Dongfeng Zeng ◽  
Zhaohua Shen ◽  
Jiali Li ◽  
...  
Keyword(s):  
High Altitude ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Inflammatory Factors ◽  
Tnf Alpha ◽  
Antibody Array ◽  
Inflammatory Factor ◽  
High Altitudes ◽  
Serum Samples ◽  
Necrosis Factor Alpha

High-altitude polycythemia (HAPC) is a common aspect of chronic mountain sickness (CMS) caused by hypoxia and is the main cause of other symptoms associated with CMS. However, its pathogenesis and the mechanisms of high-altitude acclimation have not been fully elucidated. Exposure to high altitude is associated with elevated inflammatory mediators. In this study, the subjects were recruited and placed into a plain control (PC) group, plateau control (PUC) group, early HAPC (eHAPC) group, or a confirmed HAPC (cHAPC) group. Serum samples were collected, and inflammatory factors were measured by a novel antibody array methodology. The serum levels of interleukin-2 (IL-2), interleukin-3 (IL-3), and macrophage chemoattractant protein-1 (MCP-1) in the eHAPC group and the levels of interleukin-1 beta (IL-1 beta), IL-2, IL-3, tumor necrosis factor-alpha (TNF-alpha), MCP-1, and interleukin-16 (IL-16) in the cHAPC group were higher than those in the PUC group. More interestingly, the expression of IL-1 beta, IL-2, IL-3, TNF-alpha, MCP-1, and IL-16 in the PUC group showed a remarkable lower value than that in the PC group. These results suggest that these six factors might be involved in the pathogenesis of HAPC as well as acclimation to high altitudes. Altered inflammatory factors might be new biomarkers for HAPC and for high-altitude acclimation.

scholarly journals Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

2019 ◽  
Vol 87 (4) ◽  
pp. 34 ◽  
Author(s):  
Al-Saadi ◽  
Pang ◽  
Ima-Nirwana ◽  
Chin
Keyword(s):  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Cartilage Degeneration ◽  
Redox Status ◽  
Joint Disease ◽  
Inflammatory Factors ◽  
Current Evidence ◽  
Necrosis Factor Alpha ◽  
Joint Health ◽  
Anti Inflammatory

Osteoarthritis (OA) is a joint disease resulting from cartilage degeneration and causing joint pain and stiffness. Glucosamine exerts chondroprotective effects and effectively reduces OA pain and stiffness. This review aims to summarise the mechanism of glucosamine in protecting joint health and preventing OA by conducting a literature search on original articles. Current evidence has revealed that glucosamine exhibits anti-inflammatory effects by reducing the levels of pro-inflammatory factors (such as tumour necrosis factor-alpha, interleukin-1, and interleukin-6) and enhancing the synthesis of proteoglycans that retard cartilage degradation and improve joint function. Additionally, glucosamine improves cellular redox status, reduces OA-mediated oxidative damages, scavenges free radicals, upregulates antioxidant proteins and enzyme levels, inhibits the production of reactive oxygen species, and induces autophagy to delay OA pathogenesis. In conclusion, glucosamine prevents OA and maintains joint health by reducing inflammation, improving the redox status, and inducing autophagy in joints. Further studies are warranted to determine the synergistic effect of glucosamine with other anti-inflammatory and/or antioxidative agents on joint health in humans.

scholarly journals Bifidobacterium Infantis Ameliorates Chemotherapy-Induced Intestinal Mucositis Via Regulating T Cell Immunity in Colorectal Cancer Rats

2017 ◽  
Vol 42 (6) ◽  
pp. 2330-2341 ◽  
Author(s):  
Hui Mi ◽  
Yan Dong ◽  
Bin Zhang ◽  
Haonan Wang ◽  
Chung C.K. Peter ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
T Cell ◽  
T Cell Subsets ◽  
Intestinal Villus ◽  
Villus Height ◽  
Bifidobacterium Infantis ◽  
Relative Expression ◽  
Chemotherapy Group ◽  
Tnf Α ◽  
Intestinal Mucositis

Background/Aims: Intestinal mucositis (IM) is a commonly encountered side effect in cancer patients receiving chemotherapy. This study aimed to investigate the effect of Bifidobacterium infantis (B. infantis) in attenuating the severity of chemotherapy-induced intestinal mucositis by regulating the T cell subsets in rats with colorectal cancer (CRC). Methods: Thirty male Sprague-Dawley (SD) rats were injected dimethyl hydrazine (DMH) subcutaneously for 10 weeks, and then injected SW480 cells in rectal mucosa to create a CRC model, and the rats were randomly divided into three groups: Control group (saline + saline), Chemotherapy group (saline + 5-FU+Oxaliplatin), B. infantis group (B. infantis + 5-FU+Oxaliplatin). IM was evaluated based on diarrhea severity, intestinal villus height, crypt depth, pro-inflammatory cytokines (IL-6, IL-1β, TNF-α), T cell subsets (CD4+ IL17A+ cells and CD4+ CD25+ Foxp3+ Tregs) and related cytokine profiles. Results: The results showed that the B. infantis group demonstrated a higher body weight (BW) and intestinal villus height and a deeper crypt depth compared to the Chemotherapy group. The level of IL-6, IL-1β and TNF-α which increased by chemotherapy, was lowered by B. infantis administration. Real time reverse transcription- polymerase chain reaction (RT-PCR) showed B. infantis reduced relative expression of Th17 and Th1 cells related cytokines, and increased relative expression of CD4+ CD25+ Foxp3+ Tregs related cytokines. Furthermore, Flow cytometry analysis showed B. infantis reduced CD4+ IL17A+ cells and increased CD4+ CD25+ Foxp3+ Tregs in mesenteric lymph nodes (MLNs) compared to the Chemotherapy group. Conclusion: B. infantis effectively attenuates chemotherapy-induced intestinal mucositis by decreasing Th1 and Th17 response and increasing CD4+ CD25+ Foxp3+ Tregs response.

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