Delivery of dexamethasone from electrospun PCL–PEO binary fibers and their effects on inflammation regulation

RSC Advances ◽  
2015 ◽  
Vol 5 (43) ◽  
pp. 34166-34172 ◽  
Author(s):  
Yan-Fang Li ◽  
Marina Rubert ◽  
Ying Yu ◽  
Flemming Besenbacher ◽  
Menglin Chen

Differences in surface topography, chemical composition, wettability and release kinetics of the anti-inflammatory drug dexamethasone among different PCL–PEO fibers collectively affected the regulation of inflammatory related gene expression.

2019 ◽  
Vol 20 (11) ◽  
pp. 918-923 ◽  
Author(s):  
Yazun Jarrar ◽  
Qais Jarrar ◽  
Mohammad Abu-Shalhoob ◽  
Abdulqader abed ◽  
Esra'a Sha'ban

Background: Mouse Udp-glucuronosyl Transferase (UGT) 2b1 is equivalent to the human UGT2B7 enzyme, which is a phase II drug-metabolising enzyme and plays a major role in the metabolism of xenobiotic and endogenous compounds. This study aimed to find the relative expression of the mouse ugt2b1 gene in the liver, kidney, and heart organs and the influence of Nonsteroidal Anti-inflammatory Drug (NSAID) administration. Methods: Thirty-five Blab/c mice were divided into 5 groups and treated with different commonly-used NSAIDs; diclofenac, ibuprofen, meloxicam, and mefenamic acid for 14 days. The livers, kidneys, and hearts were isolated, while the expression of ugt2b1 gene was analysed with a quantitative real-time polymerase chain reaction technique. Results: It was found that the ugt2b1 gene is highly expressed in the liver, and then in the heart and the kidneys. NSAIDs significantly upregulated (ANOVA, p < 0.05) the expression of ugt2b1 in the heart, while they downregulated its expression (ANOVA, p < 0.05) in the liver and kidneys. The level of NSAIDs’ effect on ugt2b1 gene expression was strongly correlated (Spearman’s Rho correlation, p < 0.05) with NSAID’s lipophilicity in the liver and its elimination half-life in the heart. Conclusion: This study concluded that the mouse ugt2b1 gene was mainly expressed in the liver, as 14-day administration of different NSAIDs caused alterations in the expression of this gene, which may influence the metabolism of xenobiotic and endogenous compounds.


2008 ◽  
Vol 49 (8) ◽  
pp. 1238-1244 ◽  
Author(s):  
L. G. Strauss ◽  
D. Koczan ◽  
S. Klippel ◽  
L. Pan ◽  
C. Cheng ◽  
...  

1997 ◽  
Vol 45 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Francesco Castelli ◽  
Giovanna Pitarresi ◽  
Vincenzo Tomarchio ◽  
Gaetano Giammona

2016 ◽  
Vol 4 (9) ◽  
pp. 1371-1380 ◽  
Author(s):  
Yifeng Peng ◽  
Liane E. Tellier ◽  
Johnna S. Temenoff

Heparin-based hydrogels enable tunable and linear release kinetics of the anti-inflammatory small molecule, crystal violet.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Claudia Alicia Castillo-Miranda ◽  
Ana Beatriz Morales-Cepeda ◽  
Carlos Fernando Castro-Guerrero ◽  
Homero Salas-Papayanopolos ◽  
Hugo Alberto Velasco-Ocejo ◽  
...  

The crystallization of nonsteroidal anti-inflammatory drug [2-(4-isobutyl-phenyl) propionic acid] ibuprofen (IBP) on a hydroxypropyl cellulose (HPC) and polyacrylamide (PAAm) gel was studied as well as the release kinetics of the drug. The IBP was crystallized on the gel surface of HPC/PAAm. It had a prismatic shape and the growth was made in an aqueous medium; the crystallinity grade of the gels HPC/PAAm and HPC/PAAm-IBU increased to 68% and to 58%, respectively. The release of IBP is performed by two means: by a non-Fickian diffusion process and by relaxation of the chains of the gel; without regard to temperature and the diffusion media, this correlates with the lower critical solution temperature (LCST) of the proposed gel. This polymer matrix provides an option for releasing nonsteroidal anti-inflammatory drugs in a temperature range of 35–39°C. Korsmeyer and Peppas mathematical model was simulated for data releases, statistically significant at 95% confidence level.


Author(s):  
Tahereh Bakhtiari ◽  
ShahinKhadem Azarian ◽  
Afshin Ghaderi ◽  
Arman Ahmadzadeh ◽  
Abbas Mirshafiey

Rheumatoid arthritis (RA) as a long-term autoimmune disease is characterized by pain, swelling and joints destruction. The therapeutic efficacy of Guluronic acid (G2013) (patented, DEU: 102016113017.6) was reported in phase I/II clinical trial in RA patients. In this study, we aimed to evaluate the effect of G2013 as a novel non-steroidal anti-inflammatory drug (NSAID) with immunosuppressive property on genes expression of anti-inflammatory and pro-inflammatory cytokines and their transcription factors in the blood sample of RA patients. This study was performed on 12 patients with RA who had an inadequate response to conventional treatments which were disease-modifying anti-rheumatic drugs (DMARDs), NSAID, and biologics. G2013 was administered orally at a dose of 500 mg twice daily for 12 weeks. Before and after the treatment of patients with drug G2013, the peripheral blood mononuclear cells (PBMCs) were isolated for evaluating the gene expression level of interleukin 10 (IL10), interleukin 22 (IL22), interferon γ (IFNγ), and transcription factors specific to the T helper cell lineages, forkhead box P3 (Fox-P3), Aryl hydrocarbon receptor (AHR) and T-box–containing protein expressed in T cells (T-bet) using the real-time PCR method. Since these cytokines have a key role in the progression of RA and disease condition expected induction of IFNγ, AHR, IL22, T-bet, and reduction of IL10, Fox-P3. Results indicated a significant reduction in the level of IFNγ, AHR and a significant induction in IL10, Fox-P3 gene expression in comparison with the control group. In conclusion; the results of this investigation showed a part of the immunological mechanism of G2013 as a novel anti-inflammatory that could reduce pro-inflammatory cytokine and their transcription factors. Furthermore, it increased the anti-inflammatory cytokine and its transcription factor (clinical trial identifier: IRCT2016092813739N5).


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