BACKGROUND: Chemotherapy-induced peripheral neuropathy is a common, dose-limiting side effect of cancer chemotherapeutic drugs. Hyperalgesia is a common component of neuropathic pain. Ginkgo biloba extract (GBE) is an oriental herbal medicine that has various pharmacological actions. In this study, we evaluated the effects of oral GBE on hyperalgesia in a rat model of vincristine-induced neuropathy. METHODS: Male Sprague-Dawley rats (200-250 g) were injected intraperitoneally with vincristine or saline (0.1 mg/kg/d) using a 5-day-on, 2-day-off schedule over 12 days. All the behavioral tests for mechanical, cold, and heat hyperalgesia were conducted before the daily injection during the course of vincristine treatment. Rats that developed hyperalgesia 14 days after vincristine injection were randomly assigned into 4 groups. Distilled water and GBE (50, 100, and 150 mg/kg) were administered, respectively, to the individual groups. We examined the hyperalgesia at preadministration and at 15, 30, 60, 90, 120, 150, and 180 minutes after oral drug administration. RESULTS: Saline injection did not have any significant effect on mechanical, cold, and heat hyperalgesia. Vincristine injection produced mechanical and cold hyperalgesia. For the GBE groups, the paw withdrawal threshold to mechanical stimuli was significantly increased and withdrawal frequency to cold stimuli was significantly reduced versus the control group dose-dependently (P < 0.05). CONCLUSIONS: This study demonstrates that oral administration of GBE is associated with a dose-dependent antihyperalgesic effect on mechanical and cold stimuli in a rat model of vincristine-induced neuropathy.
BACKGROUND: Chemotherapy-induced peripheral neuropathy is a common, dose-limiting side effect of cancer chemotherapeutic drugs. Hyperalgesia is a common component of neuropathic pain. Ginkgo biloba extract (GBE) is an oriental herbal medicine that has various pharmacological actions. In this study, we evaluated the effects of oral GBE on hyperalgesia in a rat model of vincristine-induced neuropathy. METHODS: Male Sprague-Dawley rats (200-250 g) were injected intraperitoneally with vincristine or saline (0.1 mg/kg/d) using a 5-day-on, 2-day-off schedule over 12 days. All the behavioral tests for mechanical, cold, and heat hyperalgesia were conducted before the daily injection during the course of vincristine treatment. Rats that developed hyperalgesia 14 days after vincristine injection were randomly assigned into 4 groups. Distilled water and GBE (50, 100, and 150 mg/kg) were administered, respectively, to the individual groups. We examined the hyperalgesia at preadministration and at 15, 30, 60, 90, 120, 150, and 180 minutes after oral drug administration. RESULTS:Saline injection did not have any significant effect on mechanical, cold, and heat hyperalgesia. Vincristine injection produced mechanical and cold hyperalgesia. For the GBE groups, the paw withdrawal threshold to mechanical stimuli was significantly increased and withdrawal frequency to cold stimuli was significantly reduced versus the control group dose-dependently (P < 0.05). CONCLUSIONS: This study demonstrates that oral administration of GBE is associated with a dose-dependent antihyperalgesic effect on mechanical and cold stimuli in a rat model of vincristine-induced neuropathy.