Anticonvulsant effect of piperine ameliorates memory impairment, inflammation and oxidative stress in a rat model of pilocarpine-induced epilepsy

Abstract

The primary active component of black pepper is piperine, which is purified and used to treat epilepsy, achieving higher efficiency when purified. The present study was conducted to evaluate whether the anticonvulsant effect of piperine ameliorates pilocarpine-induced epilepsy, and to investigate the mechanism underlying these effects. Epilepsy was induced in Sprague Dawley rats using pilocarpine. Pilocarpine-induced epilepsy in the rats was treated with 40 mg/kg piperine for 45 consecutive days. Status epilepticus and a Morris water maze test were used to analyze the anticonvulsant effects of piperine in the epileptic rats. Inflammation and oxidative stress were then measured using commercially-available kits following piperine treatment. Lastly, the activity of caspase-3 and the protein expression levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were evaluated using commercially-available kits and western blot analysis, respectively. The results demonstrated that treatment with piperine was able to reduce the status epilepticus and prevented memory impairment following pilocarpine-induced epilepsy in rats. The anticonvulsant effects of piperine decreased inflammation and oxidative stress following pilocarpine-induced epilepsy in rats. The upregulated activity of caspase-3 and expression levels of Bax/Bcl-2 were suppressed following treatment with piperine in the rats with pilocarpine-induced epilepsy. These results suggest that the anticonvulsant effects of piperine ameliorate memory impairment, inflammation and oxidative stress in a rat model of pilocarpine-induced epilepsy.

Linagliptin, the dipeptidyl peptidase‐4 enzyme inhibitor, lessens CHOP and GRP78 biomarkers levels in cisplatin‐induced neurobehavioral deficits: A possible restorative gateway

“…[ 39 ] Notably, targeting both ER stress and OS are thought to be more efficacious therapeutic options, owing to the evidence that both stresses articulate a vicious circle accentuating each other in a positive feed‐forward loop, which disturbs cell functions and activates proapoptotic signaling in numerous neurological disorders. [ 40 ]…”

Piperine-A Major Principle of Black Pepper: A Review of Its Bioactivity and Studies

“…Based on the described results, the cognitive-enhancing effect of piperine was attributed to its positive effects on the redox balance of CSF and HC neurons [114]. In a pilocarpine-induced rat model of epilepsy, administration of piperine reduced oxidative stress and inflammation and ameliorated memory impairment [91]. Piperine alone was found to produce a weak antidepressant-like effect in the tail suspension and forced swimming tests, while in combination with trans-resveratrol (tR) it enhanced its antidepressive action.…”

“…Piperine inhibits phorbol 12-myristate 13-acetate (PMA)-induced NF-κB, C/EBP, and c-Jun nuclear translocation, inhibits activation of the Akt and ERK, leading to inhibition of cyclooxygenase-2 expression in murine macrophages [90], and suppresses T cell activity and Th2 cytokine production in the ovalbumin-induced asthmatic mice [13]. In pilocarpine-induced epileptic rats, piperine exhibits anticonvulsant activity by upregulating caspase 3 and decreasing Bax/Bcl 2 [91]. Piperine lowers the serum levels of thyroxin, triiodothyronine and glucose concentrations while decreasing hepatic 5 D enzyme and glucose-6-phosphatase in adult male Swiss albino mice.…”

Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy

“…Temporal lobe epilepsy (TLE) is a clinically prevalent type of partial epilepsy. Severe head injury, stroke, intracranial infections, brain tumors, or preceding status epilepticus (SE) are factors that can induce functional and chemical changes in the brain and development of epilepsy [ 2 , 3 , 4 , 5 ]. Due to alterations occurring during epileptogenesis, patients tend to develop various comorbidities such as cognitive and psychiatric disorders, which have a detrimental impact on their quality of life [ 6 ].…”

“…Research evidence has recently outlined oxidative stress as a crucial factor responsible for cognitive dysfunction associated with TLE [ 3 , 11 , 12 ]. It is defined as an imbalance created by overproduction of free radicals and the diminished capacity of the antioxidant systems to neutralize them in the brain.…”