Abstract
Protocatechuic acid (PCA) is a type of phenolic acid found in green tea and has been shown to have potent antioxidant and anti-inflammatory properties. However, the effect of PCA on pilocarpine seizure-induced neuronal death in the hippocampus has not been evaluated. In the present study, we investigated the potential therapeutic effects of PCA on seizure-induced brain injury. Epileptic seizure was induced by intraperitoneal (i.p.) injection of pilocarpine (25 mg/kg) in adult male rats, and PCA (30 mg/kg) was injected into the intraperitoneal space for three consecutive days after the seizure. Neuronal injury and oxidative stress were evaluated three days after a seizure. To confirm whether PCA increases neuronal survival and reduced oxidative injury in the hippocampus, we performed Fluoro-Jade-B (FJB) staining to detect neuronal death and 4-hydroxynonenal (4HNE) staining to detect oxidative stress after the seizure. In the present study, we found that, compared to the seizure vehicle-treated group, PCA administration reduced neuronal death and oxidative stress in the hippocampus. To verify whether a decrease of neuronal death by PCA treatment was due to reduced glutathione (GSH) concentration, we measured glutathione with N-ethylmaleimide (GS-NEM) levels in hippocampal neurons. A seizure-induced reduction in the hippocampal neuronal GSH concentration was preserved by PCA treatment. We also examined whether microglia activation was affected by the PCA treatment after a seizure, using CD11b staining. Here, we found that seizure-induced microglia activation was significantly reduced by the PCA treatment. Therefore, the present study demonstrates that PCA deserves further investigation as a therapeutic agent for reducing hippocampal neuronal death after epileptic seizures.
Highlights
Epileptic seizures can lead to the development of several neurological disorders such as cognitive impairment [1,2,3]
To assess whether Protocatechuic acid (PCA) treatment exhibits neuroprotective effects, we evaluated the number of degenerating neurons by Fluoro-Jade-B (FJB) staining three days after a seizure
DiscussIniotnhis study, we evaluated the effects of PCA on neuronal death after a pilocarpine-induced Isneitzhuirse.sTtuhde yn,ewureopervoateluctaivteedeftfhecetsefoffecPtCsAofhPavCeAalroenadnyeubereonnatelsdteedatinh iasfctheermaiapailnodcaPraprkinines-oinnd’suced seizudnreois.teTapshreeemvniooeduuserllysop[2br5eo,e2tne6]c.etHivvaoelwueaeftvfeeedcr.,tstThhoeefePfpfCerceAtsseonhftatvrseetuaatdilnyrgetapedsiltyoecdbaerwpeinhneett-ehisnetdreudhcieipndpsoiescicazhmuerpmeasliwaniaethnurdPoCnPAadrhekaaivtnheson’s diseafsoellomwoidngelas p[i2lo5c,2a6rp].ineH-ionwduecveedr,setihzeureefifsercetdsuocfedtrtehartoiungghpPiCloAcaardpmininei-sitnradtiuocne.dWseefiozuunrdesthwatitthhePCA have PnCoAt ptrreevatimouesnltysbheoewnedevnaeluuraotpedro.teTchtievepreefsfeecntst stthuroduygthesttheed rwedhuectthioenr hoifpRpOocSamprpodaul cnteiounroannddeath followmiincgroaglpiailaocctiavraptionne,ainnduthcerodusgehizGuSrHe irsesrteodrauticoend. through PCA administration
Summary
Epileptic seizures can lead to the development of several neurological disorders such as cognitive impairment [1,2,3]. The cause of seizures has not been clearly demonstrated. A traumatic brain injury or a stroke may cause a seizure by over-activation of the excitatory synaptic neurotransmission or by downregulation of the inhibitory neurotransmission [4]. Severe and prolonged seizures can cause neuronal death, which leads to the deterioration of cognitive functions [1]. After a severe seizure, many survivors still display neuronal damage and cognitive decline. ROS usually plays an important role in the aging process of the brain and is implicated in several neurodegenerative disorders, such as stroke, Parkinson’s disease, and Alzheimer’s disease. While the precise role that ROS plays in seizure-induced neuronal death remains to be defined, its general characteristic in such neuronal death is supported in part by the investigations of spontaneous seizures [6]: Free radical scavenging and reducing ROS production decreased neuronal death after seizures [7]
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