Increased substance P and tumor necrosis factor-α level in the paws following formalin injection in rat tail

2004 ◽  
Vol 1019 (1-2) ◽  
pp. 255-258 ◽  
Author(s):  
Mauro Bianchi ◽  
Cataldo Martucci ◽  
Gabriele Biella ◽  
Paolo Ferrario ◽  
Paola Sacerdote



Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto

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.







Open Medicine ◽  
2010 ◽  
Vol 5 (2) ◽  
pp. 165-171
Author(s):  
Sami Karapolat ◽  
Bilgehan Erkut

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.



Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1215-1219 ◽  
Author(s):  
Alessandra Ferrajoli ◽  
Michael J. Keating ◽  
Taghi Manshouri ◽  
Francis J. Giles ◽  
Amanda Dey ◽  
...  

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.



Retina ◽  
2011 ◽  
Vol 31 (7) ◽  
pp. 1412-1420 ◽  
Author(s):  
Aditi Sen ◽  
Suman K Paine ◽  
Imran H Chowdhury ◽  
Amrita Mukherjee ◽  
Subhadip Choudhury ◽  
...  


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