Neuroprotective Effect ofUncaria rhynchophyllain Kainic Acid-Induced Epileptic Seizures by Modulating Hippocampal Mossy Fiber Sprouting, Neuron Survival, Astrocyte Proliferation, and S100B Expression

Chung-Hsiang Liu,Yi-Wen Lin,Nou-Ying Tang,Hsu-Jan Liu,Ching-Liang Hsieh

doi:10.1155/2012/194790

Abstract

Uncaria rhynchophylla (UR), which is a traditional Chinese medicine, has anticonvulsive effect in our previous studies, and the cellular mechanisms behind this are still little known. Because of this, we wanted to determine the importance of the role of UR on kainic acid- (KA-) induced epilepsy. Oral UR for 6 weeks can successfully attenuate the onset of epileptic seizure in animal tests. Hippocampal mossy fiber sprouting dramatically decreased, while neuronal survival increased with UR treatment in hippocampal CA1 and CA3 areas. Furthermore, oral UR for 6 weeks significantly attenuated the overexpression of astrocyte proliferation and S100B proteins but not γ-aminobutyric acid A (GABAA) receptors. These results indicate that oral UR for 6 weeks can successfully attenuate mossy fiber sprouting, astrocyte proliferation, and S100B protein overexpression and increase neuronal survival in KA-induced epileptic rat hippocampus

Highlights

Epilepsy is characterized as a condition of brain imbalance, especially in the hippocampus, with unpredictable discharge and seizures
These results indicate that oral Uncaria rhynchophylla (UR) for 6 weeks can successfully attenuate mossy fiber sprouting, astrocyte proliferation, and S100B protein overexpression and increase neuronal survival in KAinduced epileptic rat hippocampus
When UR was used to reduce KAinduced symptoms, the results indicated that the administration of oral UR for 6 weeks attenuated astrocyte proliferation in the hippocampus (Figure 4(i)), especially in the CA1, CA3, and Hilus areas (Figures 4(j)–4(l)), 58.0 ± 7.1%, 28.3 ± 4.6%, and 72.3 ± 5.1% astrocyte/field, n = 6, resp.) Serial results implied that astrocyte proliferation increased in the kainic acid- (KA-)induced group and that oral application of UR can reverse this phenomenon

Summary

Introduction

Epilepsy is characterized as a condition of brain imbalance, especially in the hippocampus, with unpredictable discharge and seizures. 30% of patients with uncontrolled seizures and using current antiepileptic drugs do not have curative therapy. Many antiepileptic drugs act as antiexcitatory or inhibitory agents to suppress seizure occurrence. These results in side effects on cognition and memory [1]. Activation of KA subtype of glutamate receptors by glutamate or KA have been reported to contribute to the epilepsy process. Recent scientific studies have indicated that intraperitoneal (i.p.) injection of KA can successfully induce epilepsy in both rats and mice with accompanying phenomena similar to that in human temporal lobe epilepsy [2]

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Conclusion