Pharmacokinetic Interaction of Ginkgo Biloba with Carbamazepine

Ginkgo biloba L. (Ginkgoaceae) usage has recently gained interest among herbalists and modern medical practitioners because of its unique pharmacological actions that are attributed to active substances such as flavonoids and terpenoids [1]. It is commonly prescribed for improvement of cerebral circulation, memory improvement and antioxidant activity. Epileptics have a greater chance of oxidative stress and memory impairment. G. biloba can be used as an alternative remedy in specific conditions such as oxidative stress and memory impairment [2]. This study aims to evaluate the pharmacokinetic interaction between the aqueous extract of Ginkgo biloba and carbamazepine. Two groups of animals, each containing 6 animals were used. The Group 1 and Group 2 received pretreatment with two different doses of extract for 7 days and on day 8 the extract was co – administered with carbamazepine. The Group 3 (control) received carbamazepine alone on day 8. The blood samples were collected for 24 hours. Samples were analyzed by HPLC [3] and pharmacokinetic parameters were calculated. Analysis of the data reveals that there was very significant decrease (p < 0.05) in the C max (4.32 ± 0.24 µg/ml), AUC total (20.31 ± 1.41 µg/ml h)and AUC 0 to n (18.31 ± 1.06 µg/ml h) of Group 1 when compared to C max (6.76 ± 0.40 µg/ml), AUC total (36.79 ± 1.57 µg/ml h) and AUC 0 to n (34.81 ± 1.23 µg/ml h) of control. There was also a significant decrease in the C max (3.51 ± 0.28 µg/ml), AUC total (11.60 ± 0.93 µg/ml h), AUC 0 to n (10.33 ± 0.82 µg/ml h), and MRT(3.53 ± 0.24 h) of Group 2 when compared to C max (6.76 ± 0.40 µg/ml), AUC total (36.79 ± 1.57 µg/ml h), AUC 0 to n (34.81 ± 1.23 µg/ml h) and MRT(5.59 ± 0.24 h) of control. There was no significant difference in the t 1/2 of the drug in both study groups when compared with control. This data suggest that Ginkgo biloba reduced the bioavailability and increased the rate of elimination of carbamazepine which confirms that there is significant herb-drug interaction between the two. References: [1] Kleijnen J, Knipschild P, (1992), Lancet, 340: 1136–1139. [2] Christen Y, (2004), Frontiers in Bioscience, 9: 3091–3104. [3] Kishore P, Krishna DR, (2003), Drug Research, 53: 763–768.

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