Huperzine a Ameliorates Cognitive Dysfunction and Neuroinflammation in Kainic Acid-Induced Epileptic Rats by Antioxidant Activity and Nlrp3/Caspase-1 Pathway Inhibition Publisher Pubmed



Mohsenimoghaddam P¹ ; Sadr SS² ; Roghani M³ ; Arabzadeh S⁴ ; Khamse S¹ ; Zamani E¹ ; Hosseini M¹ ; Moradi F⁵
Source: Clinical and Experimental Pharmacology and Physiology Published:2019

Abstract

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. © 2019 John Wiley & Sons Australia, Ltd