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Huperzine A ameliorates cognitive dysfunction and neuroinflammation in kainic acid‐induced epileptic rats by antioxidant activity and NLRP 3/caspase‐1 pathway inhibition
Author(s) -
MohseniMoghaddam Parvaneh,
Sadr Seyed Shahabeddin,
Roghani Mehrdad,
Arabzadeh Somayeh,
Khamse Safoura,
Zamani Elham,
Hosseini Marjan,
Moradi Fatemeh
Publication year - 2019
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13064
Subject(s) - malondialdehyde , kainic acid , neuroinflammation , oxidative stress , pharmacology , superoxide dismutase , chemistry , morris water navigation task , biochemistry , medicine , inflammation , hippocampus , glutamate receptor , receptor
Summary 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 ( AC hE). 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 NLRP 3 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.