Koo Byung-Soo, An Hyun-Guk, Moon Sung-Kwon, Lee Young-Choon, Kim Hyung-Min, Ko Jeong-Heon, Kim Cheorl-Ho
National Research Laboratory for Glycobiology, MOST and Department of Biochemistry and Neurobiology, College of Oriental Medicine, Dongguk University, Kyungju City, Kyungbuk, Korea.
Immunopharmacol Immunotoxicol. 2003 May;25(2):191-201. doi: 10.1081/iph-120020469.
Bombycis corpus (BC) or Bombyx Batryticatus, a batryticated silkworm and white-stiff silkworm, is a drug consisting of the dried larva of silkworm, Mobyz mori L., dead and stiffened due to the infection of Beauveria (Bals.) Vuill. In a previous paper (Kim et al., Pharmacol. Res., 43, 12-16, 2001), BC was shown to protect amyloid-beta-induced cytotoxicity. In the present study, we have found that BCE can prevent or reduce the neurotoxic actions in the hippocampus of the glutamate agonists N-methyl-D-aspartic acid (NMDA) in vitro or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid in vitro. Pre-treatment with BCE (0, 1, 2, 5, and 10 microg/ml for 6-8 h) protected primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity (0.1, 1, 10, and 50 nM/ml). BCE added either with NMDA (1 mM) or 1 h later had lesser, but still significant, protective actions. BCE also reduced NMDA-induced toxicity (1 mM). BCE (10 microg/ml) protected cultured neurons against the neurotoxic actions of either AMPA (25 microM) or kainic acid (1 mM) as well. Because the release of glutamate has been implicated in the neural damage after cerebral ischemia and other neural insults, these results suggest that BCE may contribute significantly to protect human brain to such damage.
僵蚕,即白僵蚕,是一种因被白僵菌(Bals.)Vuill.感染而死亡僵硬的家蚕幼虫制成的药物。在之前的一篇论文中(Kim等人,《药理研究》,43卷,12 - 16页,2001年),僵蚕被证明可保护β-淀粉样蛋白诱导的细胞毒性。在本研究中,我们发现僵蚕提取物(BCE)能够预防或减轻谷氨酸激动剂N-甲基-D-天冬氨酸(NMDA)体外诱导的海马神经毒性作用,以及α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)和海人酸体外诱导的神经毒性作用。用BCE(0、1、2、5和10微克/毫升,处理6 - 8小时)预处理来自胚胎第18天(E18)胚胎的原代海马培养物,可保护其免受NMDA诱导的毒性(0.1、1、10和50纳摩尔/毫升)。与NMDA(1毫摩尔)同时添加或1小时后添加BCE具有较小但仍显著的保护作用。BCE还可减轻NMDA诱导的毒性(1毫摩尔)。BCE(10微克/毫升)也能保护培养的神经元免受AMPA(25微摩尔)或海人酸(1毫摩尔)的神经毒性作用。由于谷氨酸的释放与脑缺血和其他神经损伤后的神经损伤有关,这些结果表明BCE可能对保护人脑免受此类损伤有显著作用。