The mechanism of action of
naringin has been investigated in different models of experimentally induced
cough in guinea pigs. In contrast to
codeine phosphate (6 mg/kg,
intravenous administration [i. v.]),
naringin (15, 30, and 60 mg/kg, i. v.) had no central
antitussive effect on
cough elicited by electrical stimulation of the superior laryngeal nerve.
Naringin (0.5, 1.0, and 2.0 µmol) could not prevent the
cough reflex induced by stimulation of the trachea after intracerebroventricular injection (i. c. v.), while
codeine phosphate (0.5 µmol) was highly effective. Further characterizing the peripheral mechanism of
naringin, we found that its effect (50 mg/kg, i. v.) was not affected by the depletion of sensory
neuropeptides, whereas
levodropropizine (10 mg/kg, i. v.) lost its capacity to prevent
cough in the
capsaicin-desensitized guinea pig. Furthermore, pretreatment with
glibenclamide (10 mg/kg, intraperitoneal [i. p.]) significantly reduced the
antitussive effect of
pinacidil (5 mg/kg, subcutaneous [s. c.]), but could not antagonize the
antitussive effect of
naringin (30 mg/kg, s. c.). Our present results suggest that
naringin is not a central
antitussive drug. And
naringin does not exert its peripheral
antitussive effect through either the sensory
neuropeptides system or the modulation of
ATP-sensitive K (+) channels.