scholarly journals Disease-Regulated Gene Therapy with Anti-Inflammatory Interleukin-10 Under the Control of the CXCL10 Promoter for the Treatment of Rheumatoid Arthritis

2016 ◽  
Vol 27 (3) ◽  
pp. 244-254 ◽  
Author(s):  
Mathijs G.A. Broeren ◽  
Marieke de Vries ◽  
Miranda B. Bennink ◽  
Onno J. Arntz ◽  
Arjen B. Blom ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Therapy ◽  
Interleukin 10 ◽  
Anti Inflammatory

scholarly journals Homology Modeling and Optimized Expression of Truncated IK Protein, tIK, as an Anti-Inflammatory Peptide

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4358
Author(s):  
Yuyoung Song ◽  
Minseon Kim ◽  
Yongae Kim
Keyword(s):  
Rheumatoid Arthritis ◽  
Side Effects ◽  
Homology Modeling ◽  
Protein A ◽  
Interleukin 10 ◽  
Current Treatment ◽  
Pharmaceutical Drugs ◽  
Negative Effects ◽  
Anti Inflammatory ◽  
Experimental Expression

Rheumatoid arthritis, caused by abnormalities in the autoimmune system, affects about 1% of the population. Rheumatoid arthritis does not yet have a proper treatment, and current treatment has various side effects. Therefore, there is a need for a therapeutic agent that can effectively treat rheumatoid arthritis without side effects. Recently, research on pharmaceutical drugs based on peptides has been actively conducted to reduce negative effects. Because peptide drugs are bio-friendly and bio-specific, they are characterized by no side effects. Truncated-IK (tIK) protein, a fragment of IK protein, has anti-inflammatory effects, including anti-rheumatoid arthritis activity. This study focused on the fact that tIK protein phosphorylates the interleukin 10 receptor. Through homology modeling with interleukin 10, short tIK epitopes were proposed to find the essential region of the sequence for anti-inflammatory activity. TH17 differentiation experiments were also performed with the proposed epitope. A peptide composed of 18 amino acids with an anti-inflammatory effect was named tIK-18mer. Additionally, a tIK 9-mer and a 14-mer were also found. The procedure for the experimental expression of the proposed tIK series (9-mer, 14-mer, and 18-mer) using bacterial strain is discussed.

Recent Advances for Cell / Gene Therapy in Rheumatoid Arthritis

2004 ◽  
Vol 3 (2) ◽  
pp. 119-138
Author(s):  
F. Apparailly ◽  
P. Plence ◽  
D. Noel ◽  
C. Jorgensen
Keyword(s):  
Rheumatoid Arthritis ◽  
Gene Therapy ◽  
Recent Advances ◽  
Cell Gene

Potential Effect of Anti-Inflammatory Treatment on Reducing the Cardiovascular Risk in Rheumatoid Arthritis

2012 ◽  
Vol 10 (5) ◽  
pp. 639-646 ◽  
Author(s):  
Cecilia Chighizola ◽  
Tommaso Schioppo ◽  
Francesca Ingegnoli ◽  
Pier Luigi Meroni
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Risk ◽  
Potential Effect ◽  
Anti Inflammatory

Helenalin: An Anti-Inflammatory and Anti-Neoplastic Agent: A Review

2020 ◽  
Vol 16 (8) ◽  
pp. 1134-1146
Author(s):  
Priyanka Kriplani ◽  
Kumar Guarve ◽  
Uttam S. Baghel
Keyword(s):  
Rheumatoid Arthritis ◽  
Adverse Effects ◽  
Chronic Conditions ◽  
Review Article ◽  
Google Scholar ◽  
Medical Community ◽  
Inflammatory Agent ◽  
Skin Cancers ◽  
Medicinal Properties ◽  
Anti Inflammatory

Objective: Helenalin is a natural anti-inflammatory agent that is proving its efficacy to treat various medical conditions. Though many plants are proving their effectiveness but their mechanisms are still not well understood. The objective of the review is to summarize various mechanisms of helenalin to treat inflammatory disorders and cancers, adverse effects, and avenues of further research. Methods: Structured research was carried out including Pub med, Science direct Medline, Research Gate and Google Scholar to find all articles published on helenalin. Various keywords used were “helenalin”, “Arnica”, “cancer”, “anti-inflammatory”, “cardiovascular”, “IBD”, “pharmacokinetics” etc. The aim of the review was to find out the problem prevailing in the data published to date which will help the researchers to investigate the molecule clinically. Results: Seventy articles are included in the review. Helenalin is found to cure chronic conditions like rheumatoid arthritis, ulcers and malignancies like stomach, colon, breast, larynx, lung and skin cancers via multiple mechanisms. These diseases do not proceed via a unilateral pathway. So, it can be a useful molecule to treat numerous diseases. Conclusion: This review article will help us to systemically analyze the wealth of information concerning the medicinal properties of helenalin and to recognize the gaps which have vetoed its pervasive application in the medical community.

scholarly journals Global Deletion of 11β-HSD1 Prevents Muscle Wasting Associated with Glucocorticoid Therapy in Polyarthritis

2021 ◽  
Vol 22 (15) ◽  
pp. 7828
Author(s):  
Justine M. Webster ◽  
Michael S. Sagmeister ◽  
Chloe G. Fenton ◽  
Alex P. Seabright ◽  
Yu-Chiang Lai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Skeletal Muscle ◽  
Chronic Inflammation ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Ex Vivo ◽  
Glucocorticoid Therapy ◽  
Knock Out ◽  
Fiber Size ◽  
Anti Inflammatory

Glucocorticoids provide indispensable anti-inflammatory therapies. However, metabolic adverse effects including muscle wasting restrict their use. The enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) modulates peripheral glucocorticoid responses through pre-receptor metabolism. This study investigates how 11β-HSD1 influences skeletal muscle responses to glucocorticoid therapy for chronic inflammation. We assessed human skeletal muscle biopsies from patients with rheumatoid arthritis and osteoarthritis for 11β-HSD1 activity ex vivo. Using the TNF-α-transgenic mouse model (TNF-tg) of chronic inflammation, we examined the effects of corticosterone treatment and 11β-HSD1 global knock-out (11βKO) on skeletal muscle, measuring anti-inflammatory gene expression, muscle weights, fiber size distribution, and catabolic pathways. Muscle 11β-HSD1 activity was elevated in patients with rheumatoid arthritis and correlated with inflammation markers. In murine skeletal muscle, glucocorticoid administration suppressed IL6 expression in TNF-tg mice but not in TNF-tg11βKO mice. TNF-tg mice exhibited reductions in muscle weight and fiber size with glucocorticoid therapy. In contrast, TNF-tg11βKO mice were protected against glucocorticoid-induced muscle atrophy. Glucocorticoid-mediated activation of catabolic mediators (FoxO1, Trim63) was also diminished in TNF-tg11βKO compared to TNF-tg mice. In summary, 11β-HSD1 knock-out prevents muscle atrophy associated with glucocorticoid therapy in a model of chronic inflammation. Targeting 11β-HSD1 may offer a strategy to refine the safety of glucocorticoids.

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