Attenuation of allergic airways inflammation by an extract of Hymenocardia acida

Tracheal hyperresponsiveness, airway mucus production and bronchoalveolar inflammation are the major components of asthma. Here, we aim to investigate the role in the control of asthma of a bioactive plant extracted from Hymenocardia acida in a physiological and pathophysiological model. The effect of H. acida crude extract (HACE) on total cellular components of bronchoalveolar (BAL) fluids was performed on ovalbumin (OVA) and lipopolysaccaride (LPS)-challenged Swiss mice for induction of allergic asthma and airways inflammation, respectively. Mice were pretreated with 0.9% sodium chloride (NaCl), HACE (oral doses at 100 mg/kg/body weight) for a week and then by intranasal instillation with OVA (0.5 mg/ml) + aluminium hydroxyde (20 mg/ml), during three days after intraperitoneally sensitization or with LPS (0.4 mg/ml) for a day (OVA or LPS + HACE). The BAL cells were collected in a mixed solution (0.9% NaCl and 2.6 mm Ethylenediaminetetraacetic acid EDTA) one day after the last challenge and total cells were numbered in a Neubauer chamber. The HACE: (i) significantly inhibited the airways inflammation induced by a single intranasal instillation of LPS or allergic asthma on mice challenged with 3 consecutive days intranasal instillation of OVA in comparison to control mice only instilled with 0.9% sterile. NaCl : (ii) significantly impaired the increased levels of total cells in OVA and LPS-treated mice, without changing the basal cellularity after NaCl or HACE treatment; (iii) and significantly inhibitshydroxyl radicalsandsuperoxideanions production. Taken together, these results suggest that HACE exposure induces a marked reduction of cellular component in the BAL fluid, which is only partially lymphocytes dependent.   Key words: Asthma, prevention, hymenocardia acida, mice.