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Glucosamine inhibits inducible nitric oxide synthesis
C J Meininger1, K A Kelly, H Li
1Cardiovascular Research Institute, Texas A&M University System Health Science Center, College Station, 77843, USA. cjm@tamu.edu
Biochemical and Biophysical Research Communications
|December 9, 2000
Summary
Glucosamine effectively reduces nitric oxide (NO) production by inhibiting inducible NO synthase (iNOS) protein expression. This finding supports glucosamine
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- Arthritis pathogenesis is linked to excess nitric oxide (NO) production by inducible NO synthase (iNOS).
- Glucosamine is a common treatment for arthritis in Europe.
Purpose of the Study:
- To investigate the hypothesis that glucosamine inhibits NO synthesis.
- To explore the mechanism of glucosamine's potential anti-inflammatory effects.
Main Methods:
- Utilized an in vivo rat model of lipopolysaccharide (LPS)-induced inflammation.
- Administered d-glucosamine intravenously and measured urinary nitrate excretion.
- Assessed NO production and iNOS protein expression in cultured macrophages and rat tissues.
Main Results:
- D-glucosamine administration significantly decreased urinary nitrate excretion in LPS-treated rats.
- Glucosamine dose-dependently inhibited NO production in LPS-stimulated macrophages.
- Glucosamine suppressed iNOS protein expression in macrophages and various rat organs without affecting key cofactor concentrations.
Conclusions:
- Glucosamine is a novel inhibitor of inducible NO synthesis.
- The mechanism involves the suppression of iNOS protein expression.
- Provides a biochemical rationale for using glucosamine in managing chronic inflammatory conditions like arthritis.