AIM OF THE STUDY: Kyung-Ok-Ko (KOK), a traditional herbal prescription composed of Rehmannia glutinosa var. purpurae, Panax ginseng, Poria cocos, Lycium chinense, Aquillaria agallocha and honey, has been used to treat age-related symptoms, such as amnesia or dementia, and has been shown to ameliorate scopolamine-induced memory impairment in mice. However, the effects of KOK on transient cerebral global ischemia-induced brain damage are unclear. MATERIALS AND METHODS: Transient cerebral global ischemia was induced by occluding the bilateral common carotid artery for 5 min followed by reperfusion for 7 days. KOK (0.25, 0.5, 1, or 2 g/kg) was administered orally immediately after reperfusion and once a day over the next 7 days. Y-maze or novel object recognition tasks were to analyze learning and memory capabilities at 4 or 5 days after reperfusion, respectively. Histochemistry and immunohistochemistry were used for evaluation of the effect of KOK on neuronal degeneration. RESULTS: Histochemical studies showed that KOK increased the number of viable cells detected by Nissl staining and decreased the number of degenerated neuronal cells detected by Fluoro-Jade B staining in the hippocampal CA1 region. In the immunohistochemical study, the sub-chronic KOK administration attenuated the ischemia-induced activation of microglia and astrocytes and the increase of cytokine IL-1β (P<0.05). In addition, KOK administration significantly attenuated the ischemia-induced cognitive impairments observed in the Y-maze and novel object recognition tasks (P<0.05). CONCLUSION: These findings suggest that the neuroprotective effects of KOK may be mediated by its anti-inflammatory activities, resulting in the attenuation of memory impairment.
AIM OF THE STUDY: Kyung-Ok-Ko (KOK), a traditional herbal prescription composed of Rehmannia glutinosa var. purpurae, Panax ginseng, Poria cocos, Lycium chinense, Aquillaria agallocha and honey, has been used to treat age-related symptoms, such as amnesia or dementia, and has been shown to ameliorate scopolamine-induced memory impairment in mice. However, the effects of KOK on transient cerebral global ischemia-induced brain damage are unclear. MATERIALS AND METHODS: Transient cerebral global ischemia was induced by occluding the bilateral common carotid artery for 5 min followed by reperfusion for 7 days. KOK (0.25, 0.5, 1, or 2 g/kg) was administered orally immediately after reperfusion and once a day over the next 7 days. Y-maze or novel object recognition tasks were to analyze learning and memory capabilities at 4 or 5 days after reperfusion, respectively. Histochemistry and immunohistochemistry were used for evaluation of the effect of KOK on neuronal degeneration. RESULTS: Histochemical studies showed that KOK increased the number of viable cells detected by Nissl staining and decreased the number of degenerated neuronal cells detected by Fluoro-Jade B staining in the hippocampal CA1 region. In the immunohistochemical study, the sub-chronic KOK administration attenuated the ischemia-induced activation of microglia and astrocytes and the increase of cytokine IL-1β (P<0.05). In addition, KOK administration significantly attenuated the ischemia-induced cognitive impairments observed in the Y-maze and novel object recognition tasks (P<0.05). CONCLUSION: These findings suggest that the neuroprotective effects of KOK may be mediated by its anti-inflammatory activities, resulting in the attenuation of memory impairment.