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人参皂苷对大鼠β-淀粉样蛋白诱导的失忆症的影响。

Effects of ginseng saponins on beta-amyloid-induced amnesia in rats.

作者信息

Wang Lawrence C H, Wang Beatrice, Ng Sum-Yan, Lee Tze-Fun

机构信息

Department of Biological Sciences, Biological Science Bldg., University of Alberta, Edmonton, Alta., Canada.

出版信息

J Ethnopharmacol. 2006 Jan 3;103(1):103-8. doi: 10.1016/j.jep.2005.07.010. Epub 2005 Sep 8.

Abstract

We have previously demonstrated that ginseng saponins (GS) can reverse the inhibitory effect of beta-amyloid on acetylcholine (ACh) release in the hippocampal slices. The present study was carried out to examine whether GS has any beneficial effects against amnesia induced by beta-amyloid peptides in vivo. Intracerebroventricular injection of 50 microg, but not 10 microg, beta-amyloid fragment(25-35) markedly impaired the performance of rats in avoiding a shock prod, confirming the amnesiac effect of beta-amyloid. Chronically treating the rats with GS (orally, 5 days before icv beta-amyloid injection and 7 days afterward) resulted in a dose-related improvement against beta-amyloid-induced amnesia; a significant reversion was observed at the highest GS dose (80 mg/kg/day). Post-treatment analysis on K(+)-evoked [(3)H]-ACh release from the hippocampal slices showed that beta-amyloid-treatment significantly reduced ACh release from that of the control group. However, pre-treatment with GS completely protected the animal against beta-amyloid-induced reduction of hippocampal ACh release. In contrast, treating the animals with the same optimal dose of GS and duration but only after icv beta-amyloid injection was found to be ineffective in obliterating beta-amyloid's amnesiac effect. Taken together, these observations indicated that GS pre-treatment can functionally prevent the beta-amyloid-induced memory loss possibly by minimizing the inhibitory effect of beta-amyloid on hippocampal cholinergic transmission.

摘要

我们之前已经证明人参皂苷(GS)可以逆转β-淀粉样蛋白对海马脑片乙酰胆碱(ACh)释放的抑制作用。本研究旨在探讨GS在体内对β-淀粉样肽诱导的失忆是否有任何有益作用。脑室内注射50微克而非10微克的β-淀粉样蛋白片段(25-35)显著损害大鼠躲避电击刺激的能力,证实了β-淀粉样蛋白的失忆作用。用GS长期治疗大鼠(口服,在脑室内注射β-淀粉样蛋白前5天及之后7天)可剂量依赖性地改善β-淀粉样蛋白诱导的失忆;在最高GS剂量(80毫克/千克/天)时观察到显著的逆转。对海马脑片K⁺诱发的[³H]-ACh释放进行治疗后分析表明,β-淀粉样蛋白处理显著降低了ACh释放,与对照组相比有差异。然而,GS预处理完全保护动物免受β-淀粉样蛋白诱导的海马ACh释放减少。相反,在脑室内注射β-淀粉样蛋白后,用相同最佳剂量和持续时间的GS处理动物,发现对消除β-淀粉样蛋白的失忆作用无效。综上所述,这些观察结果表明,GS预处理可能通过最小化β-淀粉样蛋白对海马胆碱能传递的抑制作用,在功能上预防β-淀粉样蛋白诱导的记忆丧失。

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