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Effects of Ginkgo biloba extract on acute cerebral ischemia in rats analyzed by magnetic resonance spectroscopy.

Hai Peng, LI Yue-fen, Sun Sheng-gang

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Abstract

AIM: To study the effect of Ginkgo biloba extract (GbE) on acute cerebral ischemia in rats. METHODS: The rats were randomly divided into four groups: sham-operated group (group I as control), ischemic group (group II), the prophylactic (GbE premedication) group (group III) and GbE-treatment group (group IV). Magnetic resonance spectroscopy (MRS) was carried out to dynamically monitor the changes in biochemical metabolic variations 48 h after cerebral ischemia and effects of GbE (100 mg/kg, ip, qd). RESULTS: (1) Lactate (Lac) peak could be detectable at the infarction area 90 min after acute cerebral ischemia and increased with time. Lac peak in the prophylactic group was elevated slightly (P<0.01, n=6), whereas in the treatment group the elevation of Lac was more remarkable than that in the prophylactic group (P<0.05, n=6). (2) In the ischemic group, the level of N-acetyl aspartate (NAA) was decreased within 4 h after ischemia (P<0.05, n=6), and the decline persisted (P<0.01, n=6). In the treatment group and prophylactic group, NAA was decreased slightly after 24 h (P<0.05, n=6). (3)Twenty-four hours after ischemia, in both ischemic group and treatment group, choline (Cho) was elevated slightly (P<0.05, n=6) and creatine (Cr) was decreased slightly (P<0.05, n=6), but in the prophylactic group these changes occurred only after 48 h. CONCLUSION: GbE could prevent and treat acute cerebral ischemia. The effectiveness was more satisfactory when GbE was used preventively.

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AIM: To study the effect of Ginkgo biloba extract (GbE) on acute cerebral ischemia in rats. METHODS: The rats were randomly divided into four groups: sham-operated group (group I as control), ischemic group (group II), the prophylactic (GbE premedication) group (group III) and GbE-treatment group (group IV). Magnetic resonance spectroscopy (MRS) was carried out to dynamically monitor the changes in biochemical metabolic variations 48 h after cerebral ischemia and effects of GbE (100 mg/kg, ip, qd). RESULTS: (1) Lactate (Lac) peak could be detectable at the infarction area 90 min after acute cerebral ischemia and increased with time. Lac peak in the prophylactic group was elevated slightly (P<0.01, n=6), whereas in the treatment group the elevation of Lac was more remarkable than that in the prophylactic group (P<0.05, n=6). (2) In the ischemic group, the level of N-acetyl aspartate (NAA) was decreased within 4 h after ischemia (P<0.05, n=6), and the decline persisted (P<0.01, n=6). In the treatment group and prophylactic group, NAA was decreased slightly after 24 h (P<0.05, n=6). (3)Twenty-four hours after ischemia, in both ischemic group and treatment group, choline (Cho) was elevated slightly (P<0.05, n=6) and creatine (Cr) was decreased slightly (P<0.05, n=6), but in the prophylactic group these changes occurred only after 48 h. CONCLUSION: GbE could prevent and treat acute cerebral ischemia. The effectiveness was more satisfactory when GbE was used preventively.

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Available abstract

AIM: To study the effect of Ginkgo biloba extract (GbE) on acute cerebral ischemia in rats. METHODS: The rats were randomly divided into four groups: sham-operated group (group I as control), ischemic group (group II), the prophylactic (GbE premedication) group (group III) and GbE-treatment group (group IV). Magnetic resonance spectroscopy (MRS) was carried out to dynamically monitor the changes in biochemical metabolic variations 48 h after cerebral ischemia and effects of GbE (100 mg/kg, ip, qd). RESULTS: (1) Lactate (Lac) peak could be detectable at the infarction area 90 min after acute cerebral ischemia and increased with time. Lac peak in the prophylactic group was elevated slightly (P<0.01, n=6), whereas in the treatment group the elevation of Lac was more remarkable than that in the prophylactic group (P<0.05, n=6). (2) In the ischemic group, the level of N-acetyl aspartate (NAA) was decreased within 4 h after ischemia (P<0.05, n=6), and the decline persisted (P<0.01, n=6). In the treatment group and prophylactic group, NAA was decreased slightly after 24 h (P<0.05, n=6). (3)Twenty-four hours after ischemia, in both ischemic group and treatment group, choline (Cho) was elevated slightly (P<0.05, n=6) and creatine (Cr) was decreased slightly (P<0.05, n=6), but in the prophylactic group these changes occurred only after 48 h. CONCLUSION: GbE could prevent and treat acute cerebral ischemia. The effectiveness was more satisfactory when GbE was used preventively.

Key concepts: Ginkgo biloba, Ischemia, Medicine, Creatine, Anesthesia, Premedication, Internal medicine, Pharmacology

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