scholarly journals Epicatechin ameliorative effects on methotrexate-induced hepatotoxicity in mice

2021 ◽  
pp. 096032712110479
Author(s):  
Reza Azadnasab ◽  
Hadi Kalantar ◽  
Layasadat Khorsandi ◽  
Heibatullah Kalantari ◽  
Mohammad Javad Khodayar
Keyword(s):  
Interleukin 1 ◽  
Antioxidant Defense System ◽  
Immunosuppressive Drug ◽  
Activity Level ◽  
Inflammatory Factors ◽  
Necrosis Factor Alpha ◽  
Serum Factors ◽  
Inflammatory Reactions ◽  
Stress Markers ◽  
Chemotherapy Agent

Background Due to the fact that methotrexate is widely used both as an immunosuppressive drug and as a chemotherapy agent, many studies are needed to reduce the side effects of this drug on non-target organs. Purpose This study was designed to investigate the effects of epicatechin (Epi) on MTX (methotrexate)-induced hepatotoxicity in mice. Research Design After 1 week for adaptation, we randomly divided 42 male Naval Medical Research Institute mice into six groups: (I) control; (II) Epi (100 mg/kg, po); (III) MTX (20 mg/kg, i.p.) on the fifth day; and (IV, V, and VI) Epi (25, 50, and 100 mg/kg, po) + MTX (20 mg/kg, i.p.) on the fifth day. At day 10, the mice were sacrificed and serum factors, oxidative stress markers, and inflammatory cytokines were measured. Results MTX increased activity level of serum enzymes (alanine aminotransferase and aspartate aminotransferase), lipid peroxidation marker (malondialdehyde), and inflammatory factors including interleukin-1 beta, tumor necrosis factor-alpha, and nitric oxide. Furthermore, MTX decreased glutathione level and activity level of catalase, superoxide dismutase, and glutathione peroxidase. Epi was able to reduce the destructive effects of oxidative/antioxidant system imbalance and inflammatory reactions and also histopathological damage in MTX intoxicated mice. Epi pretreatment reduced liver dysfunction by improving the antioxidant defense system, anti-inflammatory effects, and alleviation of histopathological damage in MTX hepatotoxicity. Conclusions Accordingly, Epi can be used as a therapeutic agent in hepatotoxicity associated with MTX chemotherapy.

Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

2018 ◽  
Vol 44 (4) ◽  
pp. 530-538
Author(s):  
Aysun Çetin ◽  
İhsan Çetin ◽  
Semih Yılmaz ◽  
Ahmet Şen ◽  
Göktuğ Savaş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Paraoxonase 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Phenotypic Effect ◽  
Necrosis Factor Alpha ◽  
Stress Markers ◽  
Tnf Α ◽  
Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

scholarly journals Counteracting Interactions between Lipopolysaccharide Molecules with Differential Activation of Toll-Like Receptors

2002 ◽  
Vol 70 (12) ◽  
pp. 6658-6664 ◽  
Author(s):  
George Hajishengallis ◽  
Michael Martin ◽  
Robert E. Schifferle ◽  
Robert J. Genco
Keyword(s):  
Cell Line ◽  
Interleukin 1 ◽  
Signal Transduction Pathway ◽  
Reporter Cell Line ◽  
Reporter Cell ◽  
Tlr2 Expression ◽  
Necrosis Factor Alpha ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Induced Tolerance

ABSTRACT We investigated counteracting interactions between the lipopolysaccharides (LPS) from Escherichia coli (Ec-LPS) and Porphyromonas gingivalis (Pg-LPS), which induce cellular activation through Toll-like receptor 4 (TLR4) and TLR2, respectively. We found that Ec-LPS induced tolerance in THP-1 cells to subsequent tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) induction by Pg-LPS, though the reverse was not true, and looked for explanatory differential effects on the signal transduction pathway. Cells exposed to Pg-LPS, but not to Ec-LPS, displayed persisting expression of IL-1 receptor-associated kinase without apparent degradation, presumably allowing prolonged relay of downstream signals. Accordingly, cells pretreated with Pg-LPS, but not with Ec-LPS, were effectively activated in response to subsequent exposure to either LPS molecule, as evidenced by assessing nuclear factor (NF)-κB activity. In fact, Pg-LPS primed THP-1 cells for enhanced NF-κB activation and TNF-α release upon restimulation with the same LPS. This was a dose-dependent effect and correlated with upregulation of surface TLR2 expression. Furthermore, we observed inhibition of NF-κB-dependent transcription in a reporter cell line pretreated with Ec-LPS and restimulated with Pg-LPS (compared to cells pretreated with medium only and restimulated with Pg-LPS), but not when the reverse treatment was made. Although Pg-LPS could not make cells tolerant to subsequent activation by Ec-LPS, Pg-LPS inhibited Ec-LPS-induced TNF-α and IL-6 release when the two molecules were added simultaneously into THP-1 cell cultures. Pg-LPS also suppressed P. gingivalis FimA protein-induced NF-κB-dependent transcription in the 3E10/huTLR4 reporter cell line, which does not express TLR2. This rules out competition for common signaling intermediates, suggesting that Pg-LPS may block component(s) of the TLR4 receptor complex. Interactions between TLR2 and TLR4 agonists may be important in the regulation of inflammatory reactions.

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 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 Effect of Aqueous Enzymatic Extraction of Deer Oil on Its Components and Its Protective Effect on Gastric Mucosa Injury

2021 ◽  
Vol 8 ◽  
Author(s):  
Yun-Shi Xia ◽  
Yin-shi Sun ◽  
Chang Liu ◽  
Zhi-Man Li ◽  
Duo-Duo Ren ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Lipid Level ◽  
Activity Level ◽  
Raw Material ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factors ◽  
Gastric Tissue ◽  
Enzymatic Extraction ◽  
Necrosis Factor Alpha ◽  
Aqueous Enzymatic Extraction

In this study, deer suet fat was used as a raw material to study the effects of aqueous enzymatic extraction of deer oil on its components, followed by studies into the potential protective activity, and related molecular mechanisms of deer oil on ethanol-induced acute gastric mucosal injury in rats. The results show that aqueous enzymatic extraction of deer oil not only has a high extraction yield and has a small effect on the content of active ingredients. Deer oil can reduce total stomach injury. Without affecting the blood lipid level, it can reduce the oxidative stress, which is manifested by reducing the content of myeloperoxidase (MPO) and enhancing the activity level of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). It also enhances the expression of defense factors prostaglandin (E2), epidermal growth factor (EGF), and somatostatin (SS), it inhibits apoptosis evidenced by the enhanced of Bcl-2 and decreased expression of cleavage of caspase-3 and Bax. At the same time, it reduces inflammation, which is manifested by reducing the expression of IL-1β, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) gastric tissue pro-inflammatory cytokines, and enhancing the expression of anti-inflammatory factors IL-4 and IL-10, and inhibiting the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway in gastric tissue.

scholarly journals Anti-Inflammatory, Antioxidative, and Hepatoprotective Effects of TransΔ9-Tetrahydrocannabinol/Sesame Oil on Adjuvant-Induced Arthritis in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Morouj Ismail ◽  
Hiba Hasan ◽  
Youmna El-Orfali ◽  
Hanan Ismail ◽  
Ghada Khawaja
Keyword(s):  
Side Effects ◽  
Interleukin 1 ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Antioxidant Defense System ◽  
Sesame Oil ◽  
Necrosis Factor Alpha ◽  
Adjuvant Induced Arthritis ◽  
First Line Therapy ◽  
Anti Inflammatory

Rheumatoid arthritis (RA) is a painful chronic autoimmune disease affecting the joints. Its first-line therapy, Methotrexate (MTX), although effective in ameliorating the progress of the disease, induces hepatotoxicity over long-term usage. Thus, seeking natural compounds with fewer side effects could be an alternative therapeutic approach. This study aimed to investigate the anti-inflammatory, antiarthritic, and antioxidative effects of synthetictrans-Δ9-tetrahydrocannabinol (Δ9-THC) dissolved in sesame oil (Dronabinol) against MTX in adjuvant-induced arthritis (AIA) rat model. Daily oral administration of Δ9-THC/sesame oil, over a period of 21 days, was well tolerated in arthritic rats with no particular psychoactive side effects. It markedly attenuated the severity of clinical manifestations, recovered the histopathological changes in tibiotarsal joints, and repressed the splenomegaly in arthritic rats. Δ9-THC/sesame oil therapy showed similar effects to MTX in neutralizing the inflammatory process of AIA, through attenuating erythrocyte sedimentation rate (ESR) scores and proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin 1-beta (IL-1β), and interleukin-6 (IL-6) levels, to normal values. As opposed to MTX, this natural combination markedly protected the liver of arthritic rats and downregulated the induced oxidative stress by increasing the antioxidant defense system such as activities of catalase and superoxide dismutase (SOD) and levels of glutathione (GSH). These results suggest promising effects for the clinical use of Δ9-THC/sesame oil therapy in alleviating arthritic clinical signs as well as arthritis-induced liver injury.

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.

Effect of Resveratrol on NF-κB Activity in Rat Peritoneal Macrophages

2006 ◽  
Vol 34 (04) ◽  
pp. 623-630 ◽  
Author(s):  
Zhen-Hua Ma ◽  
Qing-Yong Ma ◽  
Lian-Cai Wang ◽  
Huan-Chen Sha ◽  
Sheng-Li Wu ◽  
...  
Keyword(s):  
Culture Medium ◽  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Inflammatory Factors ◽  
Future Application ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference

This study was to investigate the inhibitive effect of resveratrol (RESV) on nuclear factor kappa B (NF-κB) expression and activity induced by lipopolysaccharide (LPS) in rat peritoneal macrophages (PMA). Male Sprague-Dawley (SD) rats were randomly divided into 7 groups, including control group, LPS group and RESV I-V group. In the LPS group, PMA were incubated in DMEM containing LPS (10 μg/ml), whereas in control group, PMA were incubated in DMEM only. In the RESV I-V groups, PMA were incubated in DMEM containing LPS (10 μg/ml) and different concentrations of RESV. After 24 hours of incubation, NF-κB activity in PMA, and the levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1) and nitric oxide (NO) in the culture medium were measured. In the concentrations of 1.25-5 μg/ml, RESV had a dose- dependent inhibitive effect on NF-κB activity in PMA as well as the expressions of TNF-α, IL-1 and NO in the culture medium contrasted with the LPS group. There was no significant difference in the levels of these pro-inflammatory factors between the groups of 5 μg/ml and 10 μg/ml RESV. In conclusion, RESV has the potential for the future application of preventing inflammatory diseases involving PMA.

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