AI Article Synopsis
- The study examined the anti-epileptic effects of valepotriate and its mechanisms using various seizure models in mice.
- Valepotriate demonstrated significant anti-epileptic activity at doses of 5, 10, and 20 mg/kg, effectively prolonging sleep and altering neurotransmitter expression.
- The findings suggest that the anti-epileptic effects of valepotriate may be linked to the regulation of GABA and the reduction of neuronal cell death.
Article Abstract
Objective: This work aimed to investigate the anti-epileptic effects of valepotriate isolated from Jones and studied its possible mechanisms.
Methods: The anti-epileptic effects of valepotriate were studied using maximal electroshock-induced seizure (MES), pentylenetetrazole (PTZ)-induced epilepsy, and pentobarbital sodium-induced sleeping model in mice. The possible anti-epileptic mechanisms of valepotriate were investigated by analyzing the expressions of GABA, GABA, glutamic acid decarboxylase (GAD65), Bcl-2, and caspase-3 in the brain using Western blot assay.
Results: The results indicated that valepotriate showed significant anti-epileptic activity against MES- and PTZ-induced epilepsy at doses of 5, 10, and 20 mg/kg, and ED values for MES- and PTZ-induced epilepsy were 7.84 and 7.19 mg/kg, respectively. Furthermore, valepotriate (10 and 20 mg/kg) can significantly prolong sleeping time and shorten the latency time on the pentobarbital sodium-induced sleeping time test. Furthermore, valepotriate (5, 10, and 20 mg/kg) could significantly up-regulate the expression of GABA, GAD65, and Bcl-2 and down-regulate the expression of caspase-3, but had no significant effect on the expression of GABA.
Conclusion: The results indicated that valepotriate had anti-epileptic activity and the mechanisms might be associated with regulation of GABA and inhibition of neuronal apoptosis.
Summary: Anti-epileptic effect of valepotriate was investigated for the 1 timeValepotriate showed notable anti-epileptic activityValepotriate can significantly increase the expression of GABA, glutamic acid decarboxylase 65, and Bcl-2 and reduce the expression of caspase-3.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551374 | PMC |
| http://dx.doi.org/10.4103/0973-1296.211027 | DOI Listing |
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