scholarly journals Potential anti-inflammatory activity of low molecular weight heparin in patients with exacerbations of COPD – short report

2014 ◽  
Vol 124 (1) ◽  
pp. 46-48 ◽  
Author(s):  
Barabara Rybacka-Chabros ◽  
Aldona Pietrzak ◽  
Paweł Chabros ◽  
Janusz Milanowski

AbstractIntroduction. Anti-inflammatory, separate from anti-thrombotic activity of low molecular weight heparin, is still not well documented. Aim. We estimated the influence of enoxaparin on serum levels of tumor necrosis factor alpha, as the pro-inflammatory cytokine, and interleukin-12, as the heparin-binding, anti-inflammatory cytokine, in patients with exacerbations of chronic obstructive pulmonary disease. Material and methods. Seventy-three consecutive patients (48 males, 25 females) aged 56-75 years without thromboembolic history, were enrolled into the study. They were randomized to group who received enoxaparin in one daily dose 40 mg, or to group who did not receive it. Patients receiving oral anti-coagulants were excluded from the study. Using ELISA approach, we evaluated serum levels of tumor necrosis factor-alpha and interleukin-12 at the following periods: before the first dose of enoxaparin, after 7 days of treatment and 14 days of treatment. Serum level of the C-reactive protein was evaluated simultaneously. Results. In enoxaparin recipients statistically significant (p<0.01) decreasing of TNF-alpha serum levels (from 168.33 pg/ml in admission, to 85.67 pg/ml in the end of study) to compare enoxaparine non-recipients, was observed. Interleukin-12 serum levels were significantly higher in enoxaparine recipients both after 7 days (67.46 pg/ml) and 14 days (89.32 pg/ml) of the study (p<0.05). C-reactive proteins serum levels were significantly higher in enoxaparine non-recipients than recipients (p<0.05) in all study period. Conclusions. Enoxaparin in daily dose 40 mg, significantly depressed serum levels of TNF-alpha and promote serum levels of interleukin-12. Enoxaparin administration may be beneficial for the patients with COPD exacerbation during the first 14 days of treatment

2005 ◽  
Vol 57 (6) ◽  
pp. 667-673 ◽  
Author(s):  
James F. Leckman ◽  
Liliya Katsovich ◽  
Ivana Kawikova ◽  
Haiqun Lin ◽  
Heping Zhang ◽  
...  

Pharmaceutics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 956
Author(s):  
Yonelian Yuyun ◽  
Pahweenvaj Ratnatilaka Na Bhuket ◽  
Wiwat Supasena ◽  
Piyapan Suwattananuruk ◽  
Kemika Praengam ◽  
...  

Curcumin (CUR) has been used as adjuvant therapy for therapeutic application in the treatment of psoriasis through several mechanisms of action. Due to the poor oral bioavailability of CUR, several approaches have been developed to overcome the limitations of CUR, including the prodrug strategy. In this study, CUR was esterified with mycophenolic acid (MPA) as a novel conjugate prodrug. The MPA-CUR conjugate was structurally elucidated using FT-IR, 1H-NMR, 13C-NMR, and MS techniques. Bioavailable fractions (BFs) across Caco-2 cells of CUR, MPA, and MPA-CUR were collected for further biological activity evaluation representing an in vitro cellular transport model for oral administration. The antipsoriatic effect of the BFs was determined using antiproliferation and anti-inflammation assays against hyperproliferation of tumor necrosis factor-alpha (TNF-α)-induced human keratinocytes (HaCaT). The BF of MPA-CUR provided better antiproliferation than that of CUR (p < 0.001). The enhanced hyperproliferation suppression of the BF of MPA-CUR resulted from the reduction of several inflammatory cytokines, including IL-6, IL-8, and IL-1β. The molecular mechanisms of anti-inflammatory activity were mediated by an attenuated signaling cascade of MAPKs protein, i.e., p38, ERK, and JNK. Our results present evidence for the MPA-CUR conjugate as a promising therapeutic agent for treating psoriasis by antiproliferative and anti-inflammatory actions.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad Ali Ghaffari ◽  
Elham Mousavinejad ◽  
Forough Riahi ◽  
Masoumeh Mousavinejad ◽  
Mohammad Reza Afsharmanesh

Background. Autism spectrum disorders (ASDs) are complex disorders where the pathogenesis is not fully understood. Several proinflammatory and immunoinflammatory disturbances have been observed in the etiology of ASD. There is, however, limited knowledge on variations of adipokines in ASD. The present study aimed to analyze the serum levels of resistin, visfatin, and tumor necrosis factor-alpha (TNF-α) in children with ASD in relation to body weight, gender, and ASD severity level. Method. In total, 30 children with ASD (mean age: 7.72±2.65 y; range; 4–12 y) and 30 healthy children (mean age: 8.4±2.66 y; range: 4–12 y), including males and females, were matched for age, gender, and body mass index (BMI). Serum samples were collected, and visfatin, resistin, and TNF-α serum levels were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Result. Serum visfatin, resistin, and TNF-α levels in children with ASD were significantly higher than that in the healthy patients (p<0.05). Two significant correlations were found: a correlation between resistin and visfatin with TNF-α in children with ASD (R = 0.8 and R = 0.62, resp.) and a correlation between resistin and visfatin in children with ASD (R = 0.66). Conclusion. Higher TNF-α, resistin, and visfatin levels were found in children with ASD in comparison with controls, suggesting that elevated levels of serum proinflammatory agents may be implicated in the pathophysiology of ASD.


1995 ◽  
Vol 269 (6) ◽  
pp. G953-G960 ◽  
Author(s):  
M. Mehran ◽  
E. Seidman ◽  
R. Marchand ◽  
C. Gurbindo ◽  
E. Levy

Cytokines, important mediators of inflammation, have been shown to cause disturbances in circulating and hepatic lipid metabolism. Although the intestine plays a major role in dietary fat transport and largely contributes to plasma lipoproteins, the effects of cytokines on intestinal lipid handling remain unknown. In the present study, the modulation of lipid, apoprotein, and lipoprotein synthesis and secretion by tumor necrosis factor-alpha (TNF-alpha) was investigated in Caco-2 cells. Highly differentiated and polarized cells (20 days in culture) were incubated for 20 h with recombinant human TNF-alpha (100-500 ng/ml). No cytotoxic effect of TNF-alpha cells was observed, as indicated by the determinations of Caco-2 cell viability and monolayer transepithelial resistance. Moreover, no differences in cell maturation (sucrase activity) or cell proliferation ([3H]thymidine incorporation and cell cycle analysis) were detected between treated and control cultures. Significant inhibition of lipid secretion by TNF-alpha was observed, with the greatest reduction at 500 ng/ml. TNF-alpha significantly decreased Caco-2 cell secretion of phospholipids (22%), triglycerides (30%), and cholesteryl ester (37%). It also significantly diminished the export of newly synthesized low-density lipoproteins (LDL; 20%) and high-density lipoproteins (HDL; 13%), with a lesser effect on very low-density lipoproteins (VLDL; 3%). The lipid composition of these lipoproteins was minimally affected. De novo synthesis of apo A-I, apo B-100, and apo B-48 was also markedly reduced by TNF-alpha. Sphingomyelinase activity was not increased and cell content of sphingomyelin was not altered, suggesting that inhibitory effects on lipid and apoprotein of TNF-alpha were not mediated by the ceramide pathway. Our results indicate that TNF-alpha may play a role in modulating intestinal lipid metabolism, thus affecting circulating lipoproteins.


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