Abstract
Apamin is a minor component of bee venom and is a polypeptide with 18 amino acid residues. Although apamin is considered a neurotoxic compound that blocks the potassium channel, its neuroprotective effects on neurons have been recently reported. However, there is little information about the underlying mechanism and very little is known regarding the toxicological characterization of other compounds in bee venom. Here, cultured mature cortical neurons were treated with bee venom components, including apamin, phospholipase A2, and the main component, melittin. Melittin and phospholipase A2 from bee venom caused a neurotoxic effect in dose-dependent manner, but apamin did not induce neurotoxicity in mature cortical neurons in doses of up to 10 µg/mL. Next, 1 and 10 µg/mL of apamin were applied to cultivate mature cortical neurons. Apamin accelerated neurite outgrowth and axon regeneration after laceration injury. Furthermore, apamin induced the upregulation of brain-derived neurotrophic factor and neurotrophin nerve growth factor, as well as regeneration-associated gene expression in mature cortical neurons. Due to its neurotherapeutic effects, apamin may be a promising candidate for the treatment of a wide range of neurological diseases.
Highlights
Apamin is an 18-amino acid peptide and accounts for approximately 2–3% of the dry weight of bee venom [1,2]
We first confirmed the neurotoxicity of bee venom, melittin, phospholipase 2 (PLA2), and apamin in mature cortical neurons using a cell viability assay
There was a statistically significant increase in apamin concentration from 0.1 to 10 μg/mL (Supplementary Materials, Figure S1A). These findings show that apamin is the only safe component of bee venom for primary mature cortical neurons, whereas bee venom, melittin, and PLA2 are toxic to mature cortical neurons
Summary
Apamin is an 18-amino acid peptide and accounts for approximately 2–3% of the dry weight of bee venom [1,2]. Cumulative evidence on apamin indicates that there is an optimal therapeutic dose range for treatment, above which apamin induces neurotoxicity [8]. Several studies on the use of apamin for the treatment of Alzheimer’s disease (AD) have shown that apamin may enhance neuronal excitability, synaptic plasticity, and organ potentiation in the hippocampal region by blocking the Ca2+-activated K+ (SK) channels [9,10,11]. Recent data claim that apamin has a protective effect on dopamine neurons; it can be used to treat degenerative brain disease such as Parkinson’s diseases (PD), as well as regulate synaptic plasticity, memory, and learning [5]. Its effect on mature cortical neurons has not been evaluated. The advantage of these neurons is that they readily polarize axons and dendrites, and differentiate into mature neurons with axons, dendrites, dendritic spines, and synapses
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