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논문 기본 정보

자료유형
학술저널
저자정보
Song, Jungbin (Dept. of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University) Lee, Donghun (Dept. of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University) Kim, Young-Sik (Dept. of Science in Korean Medicine, Graduate School, Kyung Hee University) Lee, Hyun Jeong (Dept. of Science in Korean Medicine, Graduate School, Kyung Hee University) Lee, Seunggyeong (Dept. of Science in Korean Medicine, Graduate School, Kyung Hee University) Kim, Dong Kuk (R&D Center, Seoul Dairy Cooperative) Kang, Shin Ho (R&D Center, Seoul Dairy Cooperative) Shin, Yong Kook (R&D Center, Seoul Dairy Cooperative) Choi, Ho-Young (Dept. of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University) Kim, Hocheol (Dept. of Herbal Pharmacology, College of Korean Medicine, Kyung Hee University)
저널정보
대한본초학회 대한본초학회지(본초분과학회지) 대한본초학회지 제31권 제4호
발행연도
2016.1
수록면
101 - 109 (9page)

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Objectives : HT070 is a mixture of herbal extracts from root of Scutellaria baicalensis and stem bark of Eleutherococcus senticosus , which have long been used for stroke therapy in traditional Korean Medicine. The purpose of this study was to investigate the neuroprotective effects of HT070 on global cerebral ischemia and its potential mechanisms.Methods : Transient global cerebral ischemia was produced by 10 min of four-vessel occlusion (4-VO) in male Wistar rats. HT070 was administered orally at a dosage of 200 mg/kg twice at 0 and 90 min after reperfusion. Hippocampal neuronal damage was measured 7 days after reperfusion. To explore the potential mechanisms, we used hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced rat pheochromocytoma (PC12) cells as an in vitro model. PC12 cells were pretreated with HT070 for 1 h and then exposed to 100 μM H<sub>2</sub>O<sub>2</sub> for 6 h in the presence of HT070. Cell viability was measured by MTT assay and the mRNA expression of Bax, Bcl-2, iNOS and COX-2 were measured by quantitative RT-PCR.Results : Oral administration of HT070 at a dose of 200 mg/kg significantly reduced neuronal death in the hippocampal CA1 region by 13.4% as compared to the vehicle-treated group. HT070 increased cell viability, reversed the down-regulated Bcl-2 mRNA level, and suppressed the up-regulated mRNA expressions of Bax, iNOS, and COX-2 in H<sub>2</sub>O<sub>2</sub>-treated PC12 cells.Conclusions : HT070 protects against delayed neuronal death after global cerebral ischemia and its neuroprotection properties might be attributed to the inhibition of mitochondrial apoptosis and ROS-generating enzymes.

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