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Ginsenoside Rb1 prevents image navigation disability, cortical infarction, and thalamic degeneration in rats with focal cerebral ischemia

1998; Elsevier BV; Volume: 7; Issue: 1 Linguagem: Inglês

10.1016/s1052-3057(98)80015-3

1532-8511

Bo Zhang, Seiji Matsuda, Junya Tanaka, Norihiko Tateishi, Nobuji Maeda, Tong‐Chun Wen, Hui Peng, Masahiro Sakanaka,

Biological and pharmacological studies of plants

Oral administration of red ginseng powder before but not after transient forebrain ischemia prevents delayed neuronal death in gerbils. One neuroprotective molecule within red ginseng powder is ginsenoside Rb1. The mechanism of action(s) of ginsenoside Rb1 remains to be determined. We performed intracerebroventricular infusion of 0.6 μg/d ginsenoside Rb1 before or after permanent occlusion of the left middle cerebral artery in stroke-prone spontaneous hypertensive rats. Ginsenoside Rb1 significantly decreased escape latency on repeated trials of the Morris water maze test, throughout the first to fourth trial days at 2 and 4 weeks after MCA occlusion (P<.05, P<.01 or P<.001). The ratio of the infarcted area to the left hemispheric area in the groups treated with 0.6 μg/d of ginsenoside Rb1 was significantly smaller than that in the saline-treated ischemic group (P<.05 or P<.001). The continuous infusion of ginsenoside Rb1 (0.06 μg/d) was less effective and the other doses examined were ineffective in ameliorating ischemia-induced image navigation disability and reducing cortical infarct size. There were significant differences in neuron numbers in the ventroposterior thalamic nucleus and in the left-to-right ratio of the thalamic area between the saline-infused ischemic group and the ginsenoside Rb1-treated ischemic group (P<.05 or P<.01). Moreover, ginsenoside Rb1 at concentrations of 0.1 to 100 fg/mL (0.09 to 90 fM), facilitated neurite extension and rescued cortical neurons from lethal damage caused by the free radical-promoting agent FeSO4, in vitro (P<.05 or P<.01). These findings suggest that ginsenoside Rb1 protects the cerebral cortex against lethal ischemic damage possibly by acting as a neurotrophic factor-like agent and by scavenging free radicals, which are overproduced in situ during and after brain ischemia. The final link between the in vivo neuroprotective action and the in vitro neurotrophic and antioxidant activities of ginsenoside Rb1 remains to be determined. Oral administration of red ginseng powder before but not after transient forebrain ischemia prevents delayed neuronal death in gerbils. One neuroprotective molecule within red ginseng powder is ginsenoside Rb1. The mechanism of action(s) of ginsenoside Rb1 remains to be determined. We performed intracerebroventricular infusion of 0.6 μg/d ginsenoside Rb1 before or after permanent occlusion of the left middle cerebral artery in stroke-prone spontaneous hypertensive rats. Ginsenoside Rb1 significantly decreased escape latency on repeated trials of the Morris water maze test, throughout the first to fourth trial days at 2 and 4 weeks after MCA occlusion (P<.05, P<.01 or P<.001). The ratio of the infarcted area to the left hemispheric area in the groups treated with 0.6 μg/d of ginsenoside Rb1 was significantly smaller than that in the saline-treated ischemic group (P<.05 or P<.001). The continuous infusion of ginsenoside Rb1 (0.06 μg/d) was less effective and the other doses examined were ineffective in ameliorating ischemia-induced image navigation disability and reducing cortical infarct size. There were significant differences in neuron numbers in the ventroposterior thalamic nucleus and in the left-to-right ratio of the thalamic area between the saline-infused ischemic group and the ginsenoside Rb1-treated ischemic group (P<.05 or P<.01). Moreover, ginsenoside Rb1 at concentrations of 0.1 to 100 fg/mL (0.09 to 90 fM), facilitated neurite extension and rescued cortical neurons from lethal damage caused by the free radical-promoting agent FeSO4, in vitro (P<.05 or P<.01). These findings suggest that ginsenoside Rb1 protects the cerebral cortex against lethal ischemic damage possibly by acting as a neurotrophic factor-like agent and by scavenging free radicals, which are overproduced in situ during and after brain ischemia. The final link between the in vivo neuroprotective action and the in vitro neurotrophic and antioxidant activities of ginsenoside Rb1 remains to be determined.