Related Experiment Videos
Chronic inflammatory response in the rat can be blocked by bindarit
A Guglielmotti1, B Silvestrini, L Saso
1Population Council, New York, New York 10021.
Summary
Bindarit effectively reduced alpha 2-macroglobulin levels and Con A-reactivity in rats with chronic inflammation, suggesting its potential in autoimmune disease research.
Area of Science:
- Immunology and Biochemistry
- Pharmacology and Drug Discovery
Background:
- Chronic inflammation, induced by Freund's complete adjuvant in rats, elevates acute-phase proteins like alpha 2-macroglobulin and alters plasma protein Con A-reactivity.
- Bindarit, a compound known to inhibit protein denaturation and reduce arthritis response, was investigated for its effects on these inflammatory markers.
Purpose of the Study:
- To evaluate the effect of bindarit on the expression of alpha 2-macroglobulin in rats with adjuvant-induced chronic inflammation.
- To assess bindarit's impact on concanavalin A (Con A)-reactivity of plasma proteins during chronic inflammation.
Main Methods:
- Adult rats were induced with chronic inflammation using Freund's complete adjuvant.
- Bindarit was administered via a medicated diet, with indomethacin used as a reference drug.
- Alpha 2-macroglobulin concentration and Con A-reactivity of proteins were analyzed using radioimmunoassay, lectin-blots, and immuno-blots.
Main Results:
- Adjuvant-induced arthritis significantly increased alpha 2-macroglobulin concentration and Con A-reactivity in rat plasma.
- Both bindarit and indomethacin treatments reduced alpha 2-macroglobulin levels and Con A-reactivity to normal levels within 37 days.
- Chronic inflammation did not significantly alter concentrations of clusterin or testibumin.
Conclusions:
- Bindarit effectively mitigates key biochemical changes associated with chronic inflammation in rats, including elevated alpha 2-macroglobulin and altered protein glycosylation.
- The findings support bindarit's potential as a tool to investigate the link between abnormal glycosylation, protein denaturation, and autoimmune diseases.