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Anti‐inflammatory and anti‐allergic effect of rosmarinic acid (RA); inhibition of seasonal allergic rhinoconjunctivitis (SAR) and its mechanism
Author(s) -
Osakabe Naomi,
Takano Hirohisa,
Sanbongi Chiaki,
Yasuda Akiko,
Yanagisawa Rie,
Inoue KenIchiro,
Yoshikawa Toshikazu
Publication year - 2004
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.552210125
Subject(s) - tbars , rosmarinic acid , thiobarbituric acid , pharmacology , medicine , edema , reactive oxygen species , infiltration (hvac) , antioxidant , chemistry , immunology , oxidative stress , lipid peroxidation , biochemistry , physics , thermodynamics
The present study was undertaken to determine whether oral supplementation with rosmarinic acid (RA) is an effective intervention for patients with SAR. In addition, the anti‐inflammatory mechanism of RA also estimated in the ear edema models. Clinical trial: Patients were treated daily with RA (200 mg or 50 mg) or placebo for 21 days. Patients recorded symptoms daily and profiles of infiltrating cells and concentration of cytokines were measured in nasal lavage fluid. Compared to placebo, supplementation with RA resulted in a significant decrease in responder rates for each symptom. RA also significantly decreased the numbers of neutrophils and eosinophils in nasal lavage fluid. Animal Study: Topical application RA showed anti‐inflammatory activity 5‐hours after 12‐tetradecanoylphorbol 13‐acetate (TPA) treatment with marked inhibition of neutrophil infiltration. Up regulation of ICAM‐1, VCAM‐1 cyclooxygenase‐2 (COX‐2), KC and MIP‐2 by TPA were markedly reduced by pre‐treatment with extract of perilla (PE) or RA. Reactive oxygen radical production detected as thiobarbituric acid reactive substance (TBARS), lipid peroxide (LPO) and 8‐hydroxy‐2'deoxyguanosine (8OH‐dG), by double treatment of TPA was reduced by pretreatment with PE or RA. RA is an effective intervention for SAR that is mediated by inhibition of PMNL infiltration. This effect of RA is due to two independent mechanisms: inhibition of the inflammatory response and scavenging of ROS.