Citation

Wang YR, Liu RY, Wang LC, Mao HF, Chen JQ. Toxicon 2007; 50(8): 1085-1094.

Affiliation

Hunan Sports Vocational College, Changsha, Hunan 410014, PR China. douzi99@163.com

Copyright

(Copyright © 2007, Elsevier Publishing)

DOI

10.1016/j.toxicon.2007.07.020

PMID

17900647

Abstract

Neuronal injury is the most important reason for various brain injuries. Cytosolic Ca(2+) overloading has been proposed as one of the main cellular processes leading to neuronal death during cerebral ischemia. It is well accepted that Ca(2+) channel blockers can protect cerebral neurons from ischemic injury. In the present studies, we investigated the molecular mechanism for the neuro-protective effect of Huwentoxin-I (HWTX-I), a spider toxin selectively blocking N-type voltage-dependent Ca((2+)) channel, on rat models with global cerebral ischemia-reperfusion injury. Our studies demonstrated that HWTX-I could maintain the morphological stability of pyramidal cells in this model. Furthermore, HWTX-I could decrease the concentration of malon-dialdehyde, but increase the activity of superoxide dismutase and glutathione peroxidase. It also reduced the expression level of related factors of Fas and tumor necrosis factor death receptor apoptosis pathways in the hippocampus. In summary, HWTX-I has an obvious neuroprotective effect, which may act through its inhibition on a certain apoptosis pathway.

Language: en