The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

Effects of intra-arterial heparin on cytokine levels in the ischemic tissue

Open Medicine ◽  
2010 ◽  
Vol 5 (2) ◽  
pp. 165-171
Author(s):  
Sami Karapolat ◽  
Bilgehan Erkut
Keyword(s):  
Tumor Necrosis Factor ◽  
Femoral Artery ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Assay Method ◽  
Control Group ◽  
Group A ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

AbstractThe purpose of this study was to evaluate the effects of systemic and intra-arterial application of heparin by measuring tissue levels of inflammatory cytokines. Twenty-one adult male Wistar albino rats were divided into three groups (Group A, B and C). All the rats had undergone ligation of the right femoral artery with 4-0 silk suture to induce limb ischemia. Group A was the control group. In Group B, unfractionated heparin of 1500 U/kg/day was given through the tail vein for 10 days, the same dose was given to distal part of ligated right femoral artery for 10 days in Group C. On the 3rd, 5th, and 10th days, biopsies were taken from rectus femoris muscle on the ischemic extremities. Tumor necrosis factor-α, interleukin-1β, and vascular cell adhesion molecule levels in muscle tissue were measured by a standard enzyme-linked immunoabsorbent assay method. An increase in tumor necrosis factor-α level was found in all three groups throughout the duration of the experiment. The increase in Group C was statistically significant as compared with the other groups. The significant increases that occurred in tumor necrosis factor-α level as a result of intra-arterial application of heparin can be postulated to be one of the results of angiogenesis induced by the heparin in ischemic extremities. This might delay the formation of a necrosis in ischemic extremities, depending on the increased angiogenesis response by means of intra-arterial heparin application and may result in extended vitality of an extremity.

scholarly journals The clinical significance of tumor necrosis factor-α plasma level in patients having chronic lymphocytic leukemia

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1215-1219 ◽  
Author(s):  
Alessandra Ferrajoli ◽  
Michael J. Keating ◽  
Taghi Manshouri ◽  
Francis J. Giles ◽  
Amanda Dey ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Lymphocytic Leukemia ◽  
Tnf Α ◽  
The Mean ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α), a cytokine possessing pleiotropic biological activities, is produced by leukemic lymphocytes in patients with chronic lymphocytic leukemia (CLL) and acts as an autocrine and paracrine growth factor in this disease. In this study, TNF-α levels were determined in 150 patients with CLL and correlated with disease characteristics, prognostic factors, and survival. The mean TNF-α plasma concentration in the patients with CLL was significantly higher than in the healthy control population (16.4 versus 8.7 pg/mL; P < .0001). Patients having an elevated TNF-α level had more advanced Rai and Binet stage disease, higher serum β2-microglobulin (β2M) levels, a greater percentage of cells expressing CD38, and lower hemoglobin and platelet levels. Patients having chromosomal abnormalities such as 11q deletion, trisomy 12, and chromosome 17 aberrations had a higher mean TNF-α level (27.5 pg/mL) than patients having a diploid karyotype or other miscellaneous cytogenetic abnormalities (14.2 pg/mL;P < .001). The TNF-α level was a predictor of survival when the Cox proportional hazards model was used with TNF-α entered as a continuous variable (P = .0001). Also, patients having a TNF-α level above the mean value of 14 pg/mL had significantly shorter survival duration (P = .00001). The TNF-α level remained predictive of survival in Cox multivariate analysis independent of Rai staging and β2M, hemoglobin, prior therapy, white cell count, and platelet level (P = .005). We conclude that the TNF-α level serves as a prognostic factor in patients with CLL and that inhibition of TNF-α in these patients could have therapeutic importance.

scholarly journals Incidence of Toxoplasmosis in Psoriasis Patients and Possible Correlation with Tumor Necrosis Factor-α

2020 ◽  
Vol 17 (1(Suppl.)) ◽  
pp. 0214
Author(s):  
Entsar J. Saheb ◽  
Yasser A.H Al-Issa ◽  
Israa Salim Mussa ◽  
Khawla H. Zghair
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
City Hospital ◽  
Tnf Α ◽  
Medical City ◽  
Positive Rate ◽  
Factor Α ◽  
Necrosis Factor

            Toxoplasma gondii is an opportunistic parasite in immune-compromised persons. The prevalence of toxoplasmosis in psoriasis patients is investigated. In addition, the treatment effect on psoriasis patients infected with toxoplasmosis through evaluating Tumor Necrosis Factor-α (TNF-α) cytokine levels is studied. Blood samples were collected from 130 individuals who involved 60 control samples and 70 samples with psoriasis. They attended Medical City Hospital in Baghdad province from October 2017 - February 2018. Then, the anti- T. gondii antibodies (IgM and IgG) and TNF- α in the sera were determined via the enzyme linked immune-sorbent assay. The highest rate of anti-Toxoplasma IgG was in psoriasis patients before treatment, it was 45 (64.29%) compared with the control which was 33 (55.00%), while the highest sero-positive rate of T. gondii IgM in the control group was 14 (23.33%) compared with patients with psoriasis 10 (14.29%). The highest rate of toxoplasmosis was in the age group (21-30) years in psoriasis patients which was 14 (31.82%). In addition, the TNF- α levels in psoriatic patients before treatment were 180.2±2.2 µg/ml, and after treatment were 223.3±41.1 µg/ml compared with the healthy control group 90.5±1.9 µg/ml. These findings suggest that incidental rate of toxoplasmosis is higher in psoriasis patients. Thus, the incidental rate of toxoplasmosis could be considered as an indication to the high risk of psoriasis.

scholarly journals Is There a Difference between the Preoperative and Postoperative Serum Levels of Interleukin-6 and Tumor Necrosis Factor-α in Children Submitted to Adenotonsillectomy?

2021 ◽  
Author(s):  
Jose Neto Ribeiro de Souza ◽  
Fernanda de Oliveira Feitosa de Castro ◽  
Camila Lemes de Souza ◽  
Mikhael Romanholo El Cheikh ◽  
Hugo Valter Lisboa Ramos ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Recurrent Tonsillitis ◽  
Tnf Α ◽  
Factor Α ◽  
Prospective Longitudinal ◽  
Necrosis Factor

Abstract Introduction Palatine and pharyngeal tonsils are the first line of defense against pathogens. Clinically, two alterations may require surgical removal of the tonsils: hypertrophy and recurrent tonsillitis. The two conditions probably result from a dysfunction of the immune system. Objective To evaluate possible differences in the plasma levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) in patients submitted to adenotonsillectomy. Methods Prospective, longitudinal study with 25 children undergoing adenotonsillectomy separated into 3 different groups: recurrent tonsillitis (RT), composed of 7 patients; recurrent hypertrophy tonsillitis (RTTH), with 8 patients; and the tonsillar hypertrophy (TH) group, with 10 patients. Ten healthy control children (SD) were also included in the study. Peripheral blood was collected, and plasma was separated to measure the levels of TNF-α, IL-6, and IL-10. The Mann-Whitney test was used for statistical analysis. Results The plasma level of IL-6 was higher in the RT (p = 0.0394) and TH (p = 0.0009) groups, compared with the control group. The TH group also had higher levels of IL-6 than the RT group (p = 0.039). The IL-6/IL-10 ratio was higher in the RT (p = 0.029) and TH (p = 0.0005) groups compared with the control group. Between the RT and RTTH groups, the IL-6/IL-10 ratio was higher in the RT group, with a statistically significant difference (p = 0.0091). Conclusion Patients with a history of chronic tonsillitis had higher levels of IL-6, compared with the control group.

scholarly journals Dynamics of Progesterone, TNF-α, and a Metabolite of PGF2α in Blood Plasma of Beef Cows following Embryo Transfer

2014 ◽  
Vol 2014 ◽  
pp. 1-8
Author(s):  
M. C. Mason ◽  
J. Copeland ◽  
E. J. Cuadra ◽  
T. H. Elsasser ◽  
Y. Jung ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Prostaglandin F2α ◽  
Beef Cows ◽  
Retention Rates ◽  
Treatment Groups ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Lactating beef cows previously synchronized for estrus (d 0) were assigned to four treatments to assess their effectiveness in increasing blood progesterone (P4) and its effects on tumor necrosis factor-α (TNF-α) and prostaglandin F2α (PGF2α) after the transfer of embryos. At the time of transfer (d 7), cows received no treatment (control;n=16), a controlled internal drug releasing device (CIDR;n=16), human chorionic gonadotropin (hCG;n=15), or gonadotropin releasing hormone (GnRH;n=15). Blood samples were taken on d 7, 14, and 21 for analysis of P4 and tumor necrosis factor-α (TNF-α). Blood was collected (every 15 min for 2 h) in half the animals in each treatment group on d 14 and the remaining half on d 21 for analysis of prostaglandin F2α metabolite (PGFM). Retention rates were 56.2, 62.5, 46.7, and 13.3% for cows in the control, CIDR, hCG, and GnRH groups, respectively. Progesterone was greater (P≤0.05) in cows receiving hCG compared to others on d 14. Progesterone in all treatment groups increased from d 7 to d 14 and declined (P≤0.05) from d 14 to d 21. Contrary to pregnant cows, P4 and TNF-α declined from d 7 to d 21 in nonpregnant cows (P≤0.05). Although PGFM increased by d 21, there was no difference between pregnant and nonpregnant cows.

The Role of Tumor Necrosis Factor-α Promoter Genetic Variation in Takayasu Arteritis Susceptibility and Medical Treatment

2011 ◽  
Vol 38 (12) ◽  
pp. 2602-2607 ◽  
Author(s):  
NAQIANG LV ◽  
AIMIN DANG ◽  
XILIN ZHU ◽  
YING LIU ◽  
YIWEN LIU ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gene Promoter ◽  
Control Group ◽  
Promoter Polymorphisms ◽  
Chinese Han ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Tumor necrosis factor-α (TNF-α) is a multifunctional proinflammatory cytokine that influences the pathogenesis of Takayasu arteritis (TA). There is still no evidence of the relationship between TNF-α gene promoter polymorphisms and TA. We examined whether variations in the TNF-α promoter region may lead to TA susceptibility and disease progression.Methods.Five TNF-α gene promoter polymorphisms (−238G/A, −308G/A, −857C/T, −863C/A, and −1031C/T) were analyzed in 110 Chinese Han patients with TA, with a control group of 362 unrelated healthy individuals. Genotypes of TNF-α gene promoter polymorphisms were identified by direct sequencing. TNF-α plasma concentrations were determined by ELISA.Results.Our results indicated that the frequency of the −863A allele was significantly lower in the patients with TA than in the controls (18.2% vs 25.7%; p = 0.011), but the significance was lost after Bonferroni correction (pc= 0.055). The frequency of −863CA/AA genotypes was significantly lower in the patients with refractory TA than in those with the 863CC genotype (22.4% vs 44.2%; pc< 0.01). The frequency of the GGCCT haplotype was significantly higher in patients than in the controls, while the frequencies of GGCAT and GGCCC haplotypes were significantly lower in patients than in controls. The plasma TNF-α concentrations were significantly lower in the subjects carrying the −863A allele than in those without. Patients with active TA had a significant increase in plasma levels of TNF-α compared with remission patients and the control group.Conclusion.Polymorphisms of the TNF-α promoter are not associated with TA in the Chinese Han population. The A allele of the −863C/A polymorphism is associated with decreased TNF-α expression, which might affect medical treatment.

scholarly journals Etanercept, a Widely Used Inhibitor of Tumor Necrosis Factor-α (TNF- α), Prevents Retinal Ganglion Cell Loss in a Rat Model of Glaucoma

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40065 ◽  
Author(s):  
Miin Roh ◽  
Yan Zhang ◽  
Yusuke Murakami ◽  
Aristomenis Thanos ◽  
Sung Chul Lee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Ganglion Cell ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cell Loss ◽  
Retinal Ganglion ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Suppression of cerebral aneurysm formation in rats by a tumor necrosis factor–α inhibitor

2014 ◽  
Vol 120 (5) ◽  
pp. 1193-1200 ◽  
Author(s):  
Toshihiro Yokoi ◽  
Takahiro Isono ◽  
Makoto Saitoh ◽  
Yayoi Yoshimura ◽  
Kazuhiko Nozaki
Keyword(s):  
Tumor Necrosis Factor ◽  
Cerebral Aneurysm ◽  
Subcutaneous Injection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cerebral Aneurysms ◽  
Control Group ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Object Although cerebral aneurysmal subarachnoid hemorrhage is a devastating disease for humans, effective medical treatments have not yet been established. Recent reports have shown that regression of some inflammatory-related mediators has protective effects in experimental cerebral aneurysm models. This study corroborated the effectiveness of tumor necrosis factor–α (TNF-α) inhibitor for experimentally induced cerebral aneurysms in rats. Methods Five-week-old male rats were prepared for induction of cerebral aneurysms and divided into 3 groups, 2 groups administered different concentrations of a TNF-α inhibitor (etanercept), and 1 control group. One month after aneurysm induction, 7-T MRI was performed. The TNF-α inhibitor groups received subcutaneous injection of 25 μg or 2.5 μg of etanercept, and the control group received subcutaneous injection of normal saline every week. The TNF-α inhibitor administrations were started at 1 month after aneurysm induction to evaluate its suppressive effects on preexisting cerebral aneurysms. Arterial circles of Willis were obtained and evaluated 3 months after aneurysm induction. Results Rats administered a TNF-α inhibitor experienced significant increases in media thickness and reductions in aneurysmal size compared with the control group. Immunohistochemical staining showed that treatment with a TNF-α inhibitor suppressed matrix metalloproteinase (MMP)–9 and inducible nitric oxide synthase (iNOS) expression through the luminal surface of the endothelial cell layer, the media and the adventitia at the site of aneurysmal formation, and the anterior cerebral artery–olfactory artery bifurcation. Quantitative polymerase chain reaction also showed suppression of MMP-9 and iNOS by TNF-α inhibitor administration. Conclusions Therapeutic administration of a TNF-α inhibitor significantly reduced the formation of aneurysms in rats. These data also suggest that TNF-α suppression reduced some inflammatory-related mediators that are in the downstream pathway of nuclear factor-κB.

Determining Serum Haptoglobin and Proinflammatory Cytokines Concentration in the Calves Clinically Diagnosed with Pneumonitis, Pneumoenteritis and Enteritis

2021 ◽  
Author(s):  
M. Kabu ◽  
C. Uyarlar
Keyword(s):  
Tumor Necrosis Factor ◽  
Total Protein ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1 ◽  
Control Group ◽  
Serum Haptoglobin ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Background: This study aims to determine the concentration of serum haptoglobin (Hp), interleukin 1 (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) in cases of Pneumonia, Pneumoenteritis and Enteritis. Methods: 60 calves were subjected to the study and they were divided into four groups. The study group consisted of the claves diagnosed with clinical pneumonia (Group P; n=15), pneumoenteritis (Group PE; n=15) and enteritis (Group E; n=15) while the control group included the healthy calves (Group C; n=15). The measurements of the concentration of serum haptoglobin (Hp), interleukin 1 (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), Total protein (TP) and Albumin (ALB) were made by using commercial kits. Conclusion: In all infection groups (P, PE ve E), Haptoglobin concentration, serum cytokine (IL-1β, IL-6 and TNF-α) and Albumin values were found to have been higher than the control group (p≤0,005). However, there was no difference in total protein. In the light of these findings, it is suggested that routine controls for Haptoglobin and cytokine (IL-1β, IL-6 and TNF-α) concentrations would be rewarding to determine the severity of the infection, to choose the suitable treatment and to detect subclinical infections in veterinary medicine.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor
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