Neuroprotective effect of Kampo medicine against brain ischemia and its mode of action

以前，我们已经revealed that chotosan (Diao-teng-san), a Kampo formula，is effective on vascular dementia clinically, and the hooks and stems of Uncaria sinensis，一个医疗植物comprising chotosan，has a neuroproteve effect in vitro. For the purpose of clarifying their effects in vivo，我们investigated whether the oral administration of chotosan extract (CSE) or Uncaria sinensisextract (USE) reduces delayed neuronal death of pyramidal cells in the hippocampus followingischemia/reperfusion (i/rp) in gerbils. CSE or USE dissolved in drinking water and provided tothe gerbils ad libitum from 7 days prior to i/rp until 7 days after i/rp. It was found that CSE-orUSE-treatments significantly reduced pyramidal cell death in the hippocampal CA1 region at 7 daysafter i/rp. Lipid peroxide (LPO) and nitrite (no_2 ^-)/nitrate (no_3 ^-) levels of the hippocampus at48hr after i/rp in the CSE- or USE-treated groups were significantly lower than those of control.Superoxide anion (o_2 ^-) and hydroxyl radical (HO) scavenging activities in both the hippocampusand cortex without i/rp, and also at 3 hours and 7 days after i/rp，were enhanced by the administration of CSE or USE. Administrations of CSE or USE without i/rpprocedure enhanced catalase (CAT) activity but superoxide dismutase (SOD) and glutathioneperoxidase (GSH-Px) activities in the both the hippocampus and cortex. CSE elevated CAT activity in thehippocampus at 7 days and that in the cortex at 3 hours after i/rp. USE raised CAT activity in boththe hippocampus and cortex at 3小时7天after i/rp. These results suggest that the oraladministrations of CSE and USE provide a protective effect against transient ischemi -induceddelayed neuronal death by reducing oxidative damage to neuronsand one of the mechanisms may be their增强猫activity in the brain的效果。

Previously, we have revealed that chotosan (Diao-teng-san), a Kampo formula, is effective on vascular dementia clinically, and the hooks and stems of Uncaria sinensis, a medicinal plant comprising chotosan, has a neuroprotective effect in vitro. For the purpose of clarifying their effects in vivo, we investigated whether the oral administration of chotosan extract (CSE) or Uncaria sinensis extract (USE) reduces delayed neuronal death of pyramidal cells in the hippocampus following ischemia/reperfusion (i/rp) in gerbils. CSE or USE were dissolved in drinking water and provided to the gerbils ad libitum from 7 days prior to i/rp until 7 days after i/rp. It was found that CSE-or USE-treatments significantly reduced pyramidal cell death in the hippocampal CA1 region at 7 days after i/rp. Lipid peroxide (LPO) and nitrite (NO_2^-)/nitrate (NO_3^-) levels of the hippocampus at 48 hr after i/rp in the CSE- or USE-treated groups were significantly lower than those of control. Superoxide anion (O_2^-・) and hydroxyl radical (HO・) scavenging activities in both the hippocampus and cortex without i/rp, and also at 3 hours and 7 days after i/rp, were enhanced by the administration of CSE or USE. Administrations of CSE or USE without i/rp procedure enhanced catalase (CAT) activity but not superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in both the hippocampus and cortex. CSE elevated CAT activity in the hippocampus at 7 days and that in the cortex at 3 hours after i/rp. USE raised CAT activity in both the hippocampus and cortex at 3 hours and 7 days after i/rp. These results suggest that the oral administrations of CSE and USE provide a protective effect against transient ischemia-induced delayed neuronal death by reducing oxidative damage to neurons, and one of the mechanisms may be their enhancing effect on CAT activity in the brain.