Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation of Hubei Province, College of Pharmacy, Tongji Medical Center, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, Hubei Province, People's Republic of China.
J Ethnopharmacol. 2011 Mar 24;134(2):275-80. doi: 10.1016/j.jep.2010.10.062. Epub 2010 Dec 16.
Abacopterin E (AE) was isolated from Abacopteris penangiana (Hook.) Ching. This study was to elucidate its neuroprotective effects against hydrogen peroxide (H(2)O(2)) induced oxidative damage in PC12 cells and d-galactose (d-Gal) induced neurotoxicity in mice brain.
In vitro, the protective effect of AE against H(2)O(2)-induced oxidative damage in the PC12 was investigated by the method of MTT (3,(4,5-dimethylthiazole-2-yl)2,5-diphenyl-tetrazolium bromide). In vivo, the protective effect of AE against d-Gal-induced neurotoxicity in mice was studied. The mice in the model group and the AE treatment groups were injected with the d-Gal 150 mg/(kg d) for 7 weeks while the mice in the control group were injected with the same volume of saline (0.9%). From the sixth week, the treatment groups were subcutaneously injected 4 or 8 mg/(kg d) of AE. In order to explore the potential mechanism of AE's action, the mice were assessed by behavioral and electrophysiological tests at the end of the administration. Then the mice brain tissues were measured for the levels of superoxide dismutases (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA).
This study showed that AE lowered the H(2)O(2)-induced cytotoxicity, and AE significantly improved the learning and memory ability in behavioral performance. The biochemical examination revealed that AE restored the activities of SOD and GSH-Px, and attenuated the increase of MDA. Moreover, the electrophysiological analysis evidently showed that AE ameliorated the long-term potentiation (LTP).
These results suggested that AE had neuroprotective effects, and its beneficial effects may be linked with inhibiting the generation of free radical and enhancing the activities of endogenous antioxidant enzymes.
从肾蕨（Hook.）Ching 中分离出 abacopterin E（AE）。本研究旨在阐明其对过氧化氢（H 2 O 2 ）诱导的 PC12 细胞氧化损伤和半乳糖（d-Gal）诱导的小鼠脑毒性的神经保护作用。
体外，采用 MTT（3，（4，5-二甲基噻唑-2-基）2，5-二苯基四唑溴盐）法研究 AE 对 H 2 O 2 诱导的 PC12 氧化损伤的保护作用。体内，研究 AE 对 d-Gal 诱导的小鼠神经毒性的保护作用。模型组和 AE 治疗组小鼠每天腹腔注射 d-Gal 150 mg/（kg·d），共 7 周；对照组小鼠腹腔注射等体积生理盐水（0.9%）。从第 6 周开始，治疗组皮下注射 4 或 8 mg/（kg·d）AE。为了探讨 AE 作用的潜在机制，在给药结束时通过行为和电生理测试对小鼠进行评估。然后测量小鼠脑组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和丙二醛（MDA）的水平。
本研究表明，AE 降低了 H 2 O 2 诱导的细胞毒性，并显著改善了行为表现中的学习和记忆能力。生化检查显示，AE 恢复了 SOD 和 GSH-Px 的活性，并减轻了 MDA 的增加。此外，电生理分析明显显示 AE 改善了长时程增强（LTP）。
这些结果表明，AE 具有神经保护作用，其有益作用可能与抑制自由基的产生和增强内源性抗氧化酶的活性有关。
