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.

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 Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

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.

AdultBrugia malayimitochondrial and nuclear fractions impart Th1-associated sizeable protection against infective larval challenges inMastomys coucha

2009 ◽  
Vol 83 (1) ◽  
pp. 83-95 ◽  
Author(s):  
S. Shakya ◽  
A.K. Srivastava ◽  
S. Misra-Bhattacharya
Keyword(s):  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Control Group ◽  
Rodent Host ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Antibody Isotypes ◽  
Factor Alpha ◽  
Mastomys Coucha

AbstractProtective immunity to the subperiodic human filariid,Brugia malayi, was explored in the rodent host,Mastomys couchaafter vaccination with subcellular fractions derived from the adult stage of the parasite. The highest level of protection was conferred in animals vaccinated with the ‘mitochondria rich’ (MT) fraction, in which microfilaraemia and worm burden were markedly reduced by 67.2 and 65.9%, respectively, followed by the ‘nucleus rich’ (NR) fraction, showing reductions of 62 and 52.3%, respectively, over the non-immunized control group. Mastomys vaccinated with MT and NR, displayed a significant increase in the level of antigen-specific serum immunoglobulin G (IgG). The levels of IgG2a, IgG2b and IgM antibody isotypes were remarkably elevated in both the MT and NR immunized groups, while IgG1 and IgG3 levels were low. Apart from antibodies, both these fractions also led to marked antigen-specific lymphoproliferationin vitro, along with enhanced release of nitric oxide by peritoneal macrophages. There was an increased population of CD4+ and CD8a+T-cells in MT immunized animals, as measured by flow cytometry, accompanied by elevated levels of proinflammatory cytokines; interferon gamma (IFN-γ), tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in the culture supernatants of the activated splenocytes. The results suggest that both NR and MT contain proinflammatory molecules which evoke a protective Th1 type of immune response.

scholarly journals PO-241 Effects of Aerobic Exercise on Activation of Neuroglia Cell and Expression of Inflammatory Factors in Aging Rats

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Yaya Xiong ◽  
Jia Jia ◽  
Xuanming Hao
Keyword(s):  
Aerobic Exercise ◽  
Exercise Intervention ◽  
Exercise Group ◽  
Inflammatory Factors ◽  
Control Group ◽  
Sprague Dawley ◽  
Tnf Α ◽  
Significant Difference ◽  
Group A ◽  
Aging Models

Objective In recent years, aerobic exercise has been considered as a method of anti-aging. The aging mechanism in nervous system is closely related to increased activation of neuroglia cells and progressing neuroinflammation with aging.This study tried to shed some light on relationship between chronic inflammation accumulation and aerobic exercise so as to understand how exercise intervened nervous aging through inflammation. In this study, we used D- galactose aging models, applying two intervention ways: aerobic exercise during aging process, after that, to explore the changes of astrocytes, microglia and TNF-α expression. This study aims to provide certain evidence that sport plays a role in anti-aging. Methods Fifty male Sprague-Dawley rats at age of eight weeks, are randomly divided into five groups: control group(A), Aging group(S), Aging while exercising group(YS), After aging Quiet group(SA), After aging exercise group(SY). The aging groups were subcutaneously injected with D- galactose 150mg / kg / d for six weeks. Group YS do swimming exercise three times a week,once 60 minutes in the first six weeks. SY had same exercise intervention in the 7-12 week after injection. We took the hippocampus of rats in A, S, YS at the end of the sixth week, and of those in SA, SY at the end of twelfth week. tested the expression of GFAP, CD11b and TNF-α by immunohistochemical staining. Results 1.GFAP immunohistochemistry: Compared with group A,The expression of GFAP in group S, YS, SA and SY was significantly increased (P<0.01). Compared with group S, The expression of GFAP in group YS significantly decreased by 20.5% (P<0.01). There is no significant difference between group SA and SY(P > 0.05). 2.CD11b immunohistochemistry: Compared with group A, The expression of CD11b in group S, YS, SA and SY was significantly increased (P<0.01). Compared with group S, The expression of CD11b in group YS decreased by 18.4% (P < 0.05).There is no significant difference between group SA and SY(P > 0.05). 3.TNF-α Immunohistochemistry: Compared with group A,The expression of TNF-α in group S, YS, SA and SY was significantly increased (P<0.01). Compared with group S, The expression of TNF-α in group YS decreased by 30.1% (P < 0.01).There is no significant difference between group SA and SY(P > 0.05). Conclusions Exercise could effectively delay aging progression through improving neuroinflammation, but hard to reverse it, so the earlier in age to exercise, the better to delay aging.  

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 Preoperative pain aggravates postoperative cognitive deficits and hippocampal neuroinflammation in rats

2019 ◽  
Author(s):  
Xiang Gao ◽  
Xian Ding ◽  
Huan Yi ◽  
Chuan-tao Lin ◽  
Yu-ping Wang ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Inflammatory Factors ◽  
Control Group ◽  
Gamma Aminobutyric Acid ◽  
Sprague Dawley ◽  
Preoperative Pain ◽  
Pain Model ◽  
Simple Operation ◽  
Tnf Α ◽  
Operation Group

Abstract Background Perioperative neurocognitive disorder (PND) is the progressive deterioration of cognitive function after surgery. The purpose of this study was to observe the effect of preoperative pain on inflammatory factors and neuronal apoptosis in the hippocampus of rats. Methods 36 adult male Sprague-Dawley rats were randomly divided into 4 groups: the control group, the pain group, the pain+operation group, and the operation group. 6 days before the surgery, the rats received cognitive training, and the cognitive evaluation was carried out on the1, 3 and 7th days after the surgery. The rats were killed on the first, third and seventh days after the surgery (n = 3 rats/day). The cognitive function of rats was evaluated by the Morris Water Maze (MWM), and the expression levels of the pro-inflammatory cytokines interleukin 6(IL-6), Interleukin 1β(IL-1β)and Tumor Necrosis Factor-α(TNF-α), Acetylcholine(Ach)and Cyclic Adenosine monophosphate(cAMP), protein kinase A(PKA)and gamma-aminobutyric acid type A receptors(GABAA) in the hippocampus were measured on the 1st, 3rd and 7th days after the operation. Results Our results showed that the pain model rats exhibited impaired behavior on the first day (P< 0.001), and this lasted until the 7th day after the operation (P≤0.002 and P≤0. 001, respectively). Preoperative pain model rats showed a higher level of apoptosis than that shown by the simple operation rats. On the 1st, 3rd and 7th days after the operation, the protein content of IL-1β, IL-6 and TNF-α in the pain operation group was increased compared to that in the simple operation group (P<0.001). ACh, cAMP, PKA and GABAA expression in the hippocampus was decreased after operation in the preoperative pain model rats. Conclusion Preoperative pain is a key risk factor for the development of PND. The ACh-PKA-GABAA signaling pathway plays a key role in the acetylcholine pathway.

Microstructural changes and immunohistological analysis of pro-inflammatory cytokines in spleens of lipopolysaccharide-induced rats

2018 ◽  
Author(s):  
Y. B. Zhong ◽  
X. L. Zhang ◽  
M. Y. Lv ◽  
X. F. Hu ◽  
Y. Li
Keyword(s):  
Inflammatory Cytokines ◽  
Optical Density ◽  
Normal Saline ◽  
Interleukin 1 ◽  
Saline Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Lymphoid Follicles ◽  
Pro Inflammatory Cytokines

This study investigated splenic status changes in weaned Sprague-Dawley rats induced by lipopolysaccharide. There were forty 26-day-old rats selected randomly and equally divided into two groups. The treatment group received daily single doses of lipopolysaccharide, and the control group was treated with normal saline. We conducted haematoxylin-eosin staining, immunohistochemical staining and semi-quantitative optical density analysis for both groups on the 29th, 32nd, 35th and 38th days after treatment. The results indicated that splenic marginal zone in the lipopolysaccharide group was thinner or disappeared compared to that of the saline group. However, the periarterial lymphoid sheath and the diameters of splenic lymphoid follicles appeared thicker and wider than those in the saline group (P less than 0.05). The expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha was mainly localized within the periarterial lymphoid sheath and splenic lymphoid follicles in the lipopolysaccharide treated rats. The integrated optical density and the average optical density in the lipopolysaccharide group were greater than those in the normal saline treated group (P less than 0.05). In conclusion, splenic immune function is probably strengthened by altering microstructures and releasing pro-inflammatory cytokines following lipopolysaccharide treatment.

Proinflammatory cytokine levels in patients with conversion disorder

2013 ◽  
Vol 25 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Utkan Tiyekli ◽  
Okan Çalıyurt ◽  
Nimet Dilek Tiyekli
Keyword(s):  
Acute Phase ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Conversion Disorder ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
Cytokine Levels ◽  
As Stress

ObjectiveIt was aimed to evaluate the relationship between proinflammatory cytokine levels and conversion disorder both commonly known as stress regulated.MethodBaseline proinflammatory cytokine levels–[Tumour necrosis factor alpha (TNF‐α), Interleukin‐1 beta (IL‐1β), Interleukin‐6 (IL‐6)]–were evaluated with enzyme‐linked immunosorbent assay in 35 conversion disorder patients and 30 healthy controls. Possible changes in proinflammatory cytokine levels were evaluated again, after their acute phase in conversion disorder patients.ResultsStatistically significant decreased serum TNF‐α levels were obtained in acute phase of conversion disorder. Those levels increased after acute conversion phase. There were no statistically significant difference observed between groups in serum IL‐1β and (IL‐6) levels.ConclusionsStress associated with conversion disorder may suppress immune function in acute conversion phase and may have diagnostic and therapeutic value.

scholarly journals Protection of Ang1-7 througth MKK/P38MAPKs inflammatory signal pathway on TNF-α stimulated mouse HL-1 cells

2021 ◽  
Author(s):  
Xuewen Wang ◽  
Yuan Cao ◽  
Pradeep depark ◽  
Deepark Sharma ◽  
Guangping Li ◽  
...  
Keyword(s):  
Protein Expression ◽  
Signal Pathway ◽  
Inflammatory Factors ◽  
Control Group ◽  
Inflammatory Factor ◽  
Tnf Α ◽  
Significant Difference ◽  
Atrial Myocyte ◽  
Group B ◽  
Group Control Group

Abstract Background to explore the effect of Ang1-7 througth MKK/P38MAPKs inflammatory signaling pathway on TNF-α-stimulated mouse HL-1 cells. Methods Using TNF-α (100 µg/ml) to establish an inflammatory atrial fibrillation model in HL-1 cell, which derived from mouse atrial myocyte. treated HL-1 cells with different concentrations of Ang 1-7 (0.1, 1 and 10 mmol/L) and divided into 5 groups, namely A group(control group), B group(TNF ), C group(TNF + Ang 1-7 0.1 mmol/L), D group(TNF + Ang 1-7 1 mmol/L ) and E group(TNF + Ang 1-7 10 mmol/L ). Firstly, different concentrations of Ang 1-7 (0.1 mmol/L, 1 mmol/L and 10 mmol/L) were used to stimulate for half an hour, and then TNF-α (100 µg/ml) was added to stimulate for four hours. Both the cells and supernatant were collected. Cells were collected for Western Blotting to detect the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38. The supernatant was subjected to flow cytometry for detecting multi-inflammatory factors. Results Compared with the A group, the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38 was statistically significant increased after stimulation with inflammatory factors (TNF-α) (P < 0.05). After intervention with Ang 1-7, the protein expression of MKK3, MKK4, MKK6, PMMK4 and PP38 was statistically significant lower than that of B group (P < 0.05). There is no significant difference of the protein expression of P38 after stimulation with inflammatory factor (TNF-α). Compared with the A group, there was no significant difference in the protein expression of MAS after the stimulation of inflammatory factor (TNF-α). After the intervention of Ang 1-7, the protein expression of MAS was higher than that of the A group and B group, but there was no significant difference (P > 0.05). The expression of MAS protein had an increasing trend, but there was no significant difference (P > 0.05). TGF-β, TNF-α was significantly increased after stimulating factor (TNF-α) was given, but was decreased after the intervention of Ang 1-7, both there were statistically significant (P < 0.05). IL-6 also had the same trend, but there was no significant difference. Conclusion Ang1-7 througth MKK/P38MAPKs inflammatory signal pathway protected on TNF-α stimulated mouse HL-1 cells

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