Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

Abstract

Epilepsy is one of the most common and severe brain diseases. The exact cause of epilepsy is unclear. Epilepsy often occurs following brain damage, such as traumatic brain injury (TBI) and ischemia. Cerebrolysin is a porcine brain peptide that is a unique neurotropic and neuroprotective agent. Cerebrolysin has been reported to increase neuroprotective effects after TBI, ischemia, and other CNS diseases. However, the effects of cerebrolysin on seizures are not known. Therefore, this study aimed to investigate the effects of neuropeptide cerebrolysin on neuronal death in the hippocampus after a seizure. To confirm the effects of cerebrolysin, we used a pilocarpine-induced seizure animal model. Cerebrolysin (2.5 ml/kg, i.p., once per day for 7 days) was immediately injected after a seizure induction. After 1 week, we obtained brain tissues and performed staining to histologically evaluate the potentially protective effects of cerebrolysin on seizure-induced neuronal death in the hippocampus. We found that cerebrolysin decreased hippocampal neuronal death after a seizure. In addition, an increase in brain-derived neurotrophic factor (BDNF) was confirmed through Western blot analysis to further support our hypothesis. Therefore, the present study suggests that the administration of cerebrolysin can be a useful therapeutic tool for preventing neuronal death after a seizure.

The neuroprotection of cerebrolysin after spontaneous intracerebral hemorrhage through regulates necroptosis via Akt/ GSK3β signaling pathway

“…DeBoer 19 reported that poststroke CBL administration leads to recovery of motor function regardless rehabilitative training without a protective effect on stroke volume in a stroke model. In the seizure model, Kang 18 also confirmed that CBL can decrease hippocampal neuronal death after the seizure. In recent clinical studies, CBL can improve overall outcomes after moderate to severe traumatic brain injury patients 22 , 23 and was also safe, better for early rehabilitation patients after ischemic stroke 24 .…”

“…CBL is an intravenously administered small molecule peptide extracted from the porcine brain, composed of approximately 15% low molecular weight peptides and 85% amino acids in an aqueous solution and has been previously used as a nootropic drug 39 . It is a brain-specific pleiotropic agent that is proposed to target multiple pathways to improve functional recovery after neurological diseases and injuries in many central nervous system diseases [18][19][20][21][22] .…”

“…Cerebrolysin (CBL) is a small molecule peptide extracted from the porcine brain and has been previously used as a nootropic drug 18 . Increasing studies have demonstrated that CBL administration can promote recovery of motor function, improve EBI, decrease hippocampal neuronal death in basic researches [19][20][21] .…”

RIP3 Inhibition ameliorates chronic constriction injury-induced neuropathic pain by suppressing JNK signaling

“…Lastly, to confirm the therapeutic action of sinomenine, we stained for NeuN, a specific marker of living neurons [ 37 ]. The results revealed that the number of active neurons in the spinal dorsal horn was lower in CCI rats than in control rats.…”

Cerebrolysin Combined with Rehabilitation Enhances Motor Recovery and Prevents Neural Network Degeneration in Ischemic Stroke Patients with Severe Motor Deficits

“…Cerebrolysin (EVER Neuro Pharma GmbH, Unterach am Attersee, Austria, 30 mL infusion), a unique neuropeptide preparation of low-molecular-weight neuropeptides (<10 kDa) and free amino acids, has been shown to have neuroprotective and neurorestorative properties [11,12]. Cerebrolysin has been reported to increase neuroprotective effects by protecting against excitotoxicity and oxidative stress as well as modulating the inflammatory response [34]. In addition, Cerebrolysin could enhances neurogenesis and neurorestoration through the activity of the neurotrophic factor and sonic hedgehog signaling pathways [35].…”