- 영문명
- Inhibition of Oxidative Stress-induced and Excitotoxic Neuronal Cell Damage by Xuesaitong Ruanjiaonang
- 발행기관
- 대한약학회
- 저자명
- 조정숙(Jung sook Cho)
- 간행물 정보
- 『약학회지』제49권 제1호 (2005년), 30~37쪽, 전체 8쪽
- 주제분류
- 의약학 > 기타의약학
- 파일형태
- 발행일자
- 2005.02.28
국문 초록
영문 초록
Xuesaitong Ruanjiaonang (XR), a soft capsule containing Panax notoginseng saponins as main ingredients, is believed to remove extravasated blood and increase cerebral blood flow by improving blood circulation, and therefore, has been used in China to treat ischemic stroke or hemiplegia caused by cerebral thrombosis. To characterize pharmacological actions of XR, the present study evaluated its effects on neuronal cell damage induced by various oxidative insults or excitotoxic amino acids in primary cultured rat cortical cells. The neuronal cell viability was not affected by XR with the exposure for 2 h at the concentrations tested in this study (10~1000 ㎍/㎖). However, significant reduction of the cell viability was observed when the cultured cells were exposed to XR at 1000 ㎍/㎖ for 24 h. XR was found to concentration-dependently inhibit the oxidative neuronal damage induced by H2O2, xanthine/xanthine oxidase or Fe2+/ascorbic acid. In addition, it dramatically inhibited the excitotoxic damage induced by glutamate or N-methyl-D- aspartate (NMDA). We found that the NMDA-induced neurotoxicity was inhibited more effectively and potently than the glutamate-induced toxicity. Moreover, XR was found to exert mild inhibition of lipid peroxidation induced by Fe2+/ascorbic acid in rat brain homogenates and some 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity. Taken together, these results demonstrate neuroprotective and antioxidant effects of XR, showing inhibition of oxidative and excitotoxic damage in the cultured cortical neurons, as well as inhibition of lipid peroxidation and its radical scavenging activity. Considering that excitotoxicity and oxidative stress play crucial roles in neuronal cell damage during ischemia and reperfusion, these results may provide pharmacological basis for its clinical usage to treat ischemic stroke.
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