Inflammation is a protective physiological response that may cause tissue damage when prolonged. Copper–amino acid complexes, including Cu(L-alanine)₂, have been reported to possess various biological activities. However, their anti-inflammatory potential remains underexplored. This study evaluated the in vivo anti-inflammatory effects of Cu(L-ala)₂ using three experimental models in rats: acetic acid-induced peritoneal vascular permeability, carrageenan-induced paw edema, and nitric oxide (NO) production in paw tissue. Rats were divided into four groups (n = 6) and treated with vehicle control (1% DMSO), indomethacin (10 mg/kg), or Cu(L-ala)₂ at doses of 2 or 20 mg/kg. Acetic acid markedly increased vascular permeability, which was significantly inhibited by Cu(L-ala)₂ by 74.1% (2 mg/kg) and 81.23% (20 mg/kg). In the paw edema model, both doses significantly reduced inflammation compared with the control, with the 2 mg/kg dose showing the greatest inhibition (63.79%) at 1 hour. In contrast, Cu(L-ala)₂ produced only a moderate reduction in NO levels, reaching statistical significance only at 20 mg/kg (27.56%), while indomethacin showed a stronger effect (46.28%). Overall, Cu(L-ala)₂ demonstrated significant anti-inflammatory activity by reducing vascular permeability and edema formation. However, its limited effect on NO production suggests that its mechanism of action may be largely NO-independent. Further studies are required to clarify its molecular targets, dose–response behavior, and therapeutic potential.
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Jalil et al. (2026) studied this question.
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