Changquan Wang,
Guangming Xia,
Gang Li,
Feng Wan,
Yanwen Lv 
,
Zhanchi Xiao
For correspondence:- Yanwen Lv Email: Lvyanwhzcdoc@126.com
Accepted: 28 August 2018 Published: 30 September 2018
Citation: Wang C, Xia G, Li G, Wan F, Lv Y, Xiao Z. Attenuation of kainic acid-induced epilepsy by butyrate is associated with inhibition of glial activation. Trop J Pharm Res 2018; 17(9):1739-1743 doi: 10.4314/tjpr.v17i9.8
© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Purpose: To investigate the function and potential therapeutic relevance of butyrate in epilepsy using rat models of kainic acid (KA)-induced epilepsy.
Methods: The neurotoxin KA was applied to rats and rat astrocytes to establish models of epilepsy in vivo and in vitro. Multiple parameters, including behavioural seizure scores, were evaluated in rats and rat astrocytes treated with KA alone or in combination with butyrate. Western blot was performed to examine the levels of phosphorylated extracellular signal-related kinase (p-ERK), proinflammatory cytokine (IL-1ß), and glial fibrillary acidic protein (GFAP).
Results: Significant increases were observed in the seizure-related proteins p-ERK and GFAP and in the proinflammatory cytokine IL-1ß in KA-treated rats and rat astrocytes (p < 0.05). Butyrate treatment attenuated KA-induced epileptic behaviour in rats and significantly reduced the ex
Conclusion: Butyrate has potential as a treatment for epilepsy by inhibiting the activation of p-ERK, astrogliosis, and inflammation, which were induced by KA in rats and rat astrocytes.
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