Although in vitro studies have shown that
nicotinic acid inhibits some aspects of the inflammatory response, a reduced number of in vivo studies have investigated this activity. To the best of our knowledge, the effects induced by
nicotinic acid in models of nociceptive and inflammatory
pain are not known. Per os (p.o.) administration of
nicotinic acid (250, 500 or 1000 mg/kg, -1 h) inhibited the first and the second phases of the nociceptive response induced by
formalin in mice.
Nicotinic acid (250 or 500 mg/kg, -1 and 3 h) also inhibited the
mechanical allodynia induced by
carrageenan in rats, a model of inflammatory
pain. However, in a model of
nociceptive pain, exposure of mice to a hot-plate,
nicotinic acid was devoid of activity. In addition to inhibiting the nociceptive response in models of inflammatory
pain,
nicotinic acid (250 or 500 mg/kg, p.o., -1 and 3 h) inhibited paw
edema induced by
carrageenan in mice and rats.
Picolinic acid (62.5 or 125 mg/kg, p.o., -1 h), a
nicotinic acid isomer, inhibited both phases of the nociceptive response induced by
formalin, but not paw
edema induced by
carrageenan in mice. The other
nicotinic acid isomer,
isonicotinic acid, was devoid of activity in these two models. In conclusion, our results represent the first demonstration of the activity of
nicotinic acid in experimental models of nociceptive and inflammatory
pain and also provide further support to its anti-inflammatory activity. It is unlikely that conversion to
nicotinamide represents an important mechanism to explain the antinociceptive and anti-inflammatory activities of
nicotinic acid. The demonstration of new activities of
nicotinic acid, a drug that has already been approved for clinical use and presents a positive safety record, may contribute to raise the interest in conducting clinical trials to investigate its usefulness in the treatment of painful and inflammatory diseases.