Neuroprotective effects of Abacopterin E from Abacopteris penangiana against oxidative stress-induced neurotoxicity.

AIM OF THE STUDY

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.

MATERIALS AND METHODS

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).

RESULTS

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).

CONCLUSIONS

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.