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Huperzine A ameliorates cognitive dysfunction and neuroinflammation in kainic acid‐induced epileptic rats by antioxidant activity and NLRP3/caspase‐1 pathway inhibition

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Temporal lobe epilepsy (TLE) is one of the most prevalent types of epilepsy in human. Huperzine A (Hup‐A) has been reported to possess antioxidative and anti‐inflammatory properties; however, its role in TLE induced by kainic acid has not been determined. The current study investigated the protective effects of Hup‐A (0.1 mg/kg) in kainic acid‐induced model of TLE in the rat. In the current study, it was found that Hup‐A significantly prevented the seizure intensity and learning and memory deterioration which was assessed by Morris water maze (MWM) and novel object recognition task (NOR). Additionally, Hup‐A inhibited oxidative stress, inflammation, and acetylcholinesterase activity (AChE). In addition, catalase and superoxide dismutase (SOD) activities increased after Hup‐A treatment, while malondialdehyde (MDA) and nitrite levels significantly reduced. Regarding inflammation, this drug decreased kainic acid‐induced NLRP3 expression in microglial cells and caspase‐1 activity in hippocampal tissue, possibly through diminishing oxidative stress. Taken together, our data showed that Hup‐A could be a potential protective substance to ameliorate seizure severity and some memory deficits related to epilepsy via attenuating neuroinflammation and protection of neurons.
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Keywords: acetylcholinesterase; cognitive dysfunction; huperzine A; inflammasome; oxidative stress; temporal lobe epilepsy

Document Type: Research Article

Publication date: April 1, 2019

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