Anticonvulsant effect of Asparagus africanus Lam. root decoction on pilocarpine-induced temporal lobe epilepsy in white mice (Mus musculus Swiss)

Abstract

Asparagus africanus Lam. (Asparagaceae) is a widely used plant in traditional medicine as an anti-inflammatory, antioxidant, for the treatment of nervous disorders and epilepsy. The objective of this work was to study the anticonvulsant effects of A. africanus root decoction in white mice (Mus musculus Swiss) induced by pilocarpine. The experimental induction of "status epilepticus" and the evaluation of the anticonvulsant effects of A. africanus root decoction on pilocarpine-induced clonic and tonic convulsions were carried out. Seizure severity, latency, duration and number of clonics and tonics convulsions were evaluated. Concentrations of GABA, GABA-T, TNF-α and stress markers in the brains of mice were also estimated. A. africanus decreased the duration and number of clonic and tonic convulsions which increased the latency time of onset of clonic and tonic convulsions significantly and in a dose-dependent manner. GABA increased significantly in the brains of animals treated with A. africanus and a significant decrease of GABA-T and TNF-α. A. africanus also showed antioxidant effects. These results show that A. africanus has anticonvulsant effects. A. africanus would thus contain beneficial antiradical constituents in the treatment of epilepsy. These constituents would thus oppose free radicals. These results would justify the use of this plant in traditional medicine in the treatment of epilepsy.

Ameliorative Potential of (-) Pseudosemiglabrin in Mice with Pilocarpine-Induced Epilepsy: Antioxidant, Anti-Inflammatory, Anti-Apoptotic, and Neurotransmission Modulation

“…As a result of these data, epilepsy can be induced by a disruption in GABAergic and glutamatergic neurotransmission. These findings are consistent with earlier findings [ 1 , 9 , 13 , 16 , 37 , 38 ].…”

“…Astrocytes are recognized to have a role in regulating neurotransmitter concentrations, such as GABA and glutamate, as well as neuronal homeostasis and immunological response [ 5 ]. The primary inhibitory neurotransmitter in the brain is GABA, and boosting GABA neurotransmission has been proven to reduce seizures [ 9 ]. Blocking the glutamate decarboxylase enzyme, which is responsible for GABA generation from glutamate, and the SLC1A2 transporter, which is responsible for glutamate uptake, or boosting the GABA transaminase enzyme, which is responsible for GABA metabolism, and the astrocytic SLC6A1 transporter, which is the crucial brain GABA transporter that is responsible for GABA uptake, cause epilepsy [ 1 , 16 , 35 , 39 ].…”

“…Furthermore, astrocytes produce several pro-inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor-α (TNF-α), through the activation of the toll-like receptor 4/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR-4/NF-κB) cascade, which can aggravate astrogliosis and augment epileptogenic inflammatory signaling [ 6 , 7 ]. Moreover, these pro-inflammatory cytokines accumulate rapidly in this vicious loop and influence synaptic transmission, altering neuronal excitability and leading to seizure genesis, oxidative stress, neuronal apoptosis, and damage, with additional worsening of the condition [ 8 , 9 ].…”

“…Additionally, recurring seizures are associated with decreased γ-aminobutyric acid (GABA) levels, increased GABA-transaminase activity, and decreased L-glutamate decarboxylase activity in cortical and hippocampus tissue, indicating that GABAergic neurotransmission is disturbed during epilepsy [ 9 , 10 ]. Furthermore, repeated seizures cause an increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) via excitotoxicity, which changes protein function, membrane permeability, gene expression, and neuronal apoptosis [ 11 ].…”

“…Furthermore, repeated seizures cause an increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) via excitotoxicity, which changes protein function, membrane permeability, gene expression, and neuronal apoptosis [ 11 ]. These molecular dysfunctions have been linked to increased neuronal excitability, augmented pro-inflammatory cytokine levels, immune system exacerbation, and a reduction in the seizure threshold in an epilepsy patient [ 8 , 9 , 12 ].…”