Protection by petaslignolide A, a major neuroprotective compound in the butanol extract of Petasites japonicus leaves, against oxidative damage in the brains of mice challenged with kainic acid.

The neuroprotective effect of petaslignolide A (PA), a furfuran lignan isolated from butanol fraction of Petasites japonicus (Sieb. et Zucc.) Maxim. (Compositae) leaves, on the oxidative damage in the brain of mice challenged with kainic acid was examined using behavioral signs and biochemical parameters of oxidative stress. PA (40 mg/kg) was administered to ICR male mice through a gavage for 4 days consecutively, and on the final day, kainic acid (50 mg/kg) was administered intraperitoneally. During the 4-day treatment with PA, the body weight gain was not significantly different from that of vehicle-treated control animals. PA (40 mg/kg) alleviated the behavioral signs of kainic acid neurotoxicity and reduced the mortality (50%) by kainic acid to 12.5%. Moreover, the administration of PA restored the levels of glutathione and thiobarbituric acid-reactive substances as well as GSH-peroxidase activity in the brains of mice administered kainic acid to control levels (P < 0.05). In comparison, PA (40 mg/kg) was approximately comparable to the butanol fraction (200 mg/kg) of P. japonicus extract in reducing kainic acid neurotoxicity. On the basis of these results, PA is suggested to be a major neuroprotective agent primarily responsible for the protective action of the butanol fraction of P. japonicus extract against kainic acid-induced neurotoxicity in the brains of mice.