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dc.contributor.authorZhang, Shu-Hongen
dc.contributor.authorLiu, Donghaien
dc.contributor.authorHu, Qingyunen
dc.contributor.authorZhu, Jinlingen
dc.contributor.authorWang, Shuqiuen
dc.contributor.authorZhou, Shaoboen
dc.date.accessioned2019-08-19T09:19:19Z
dc.date.available2019-08-19T09:19:19Z
dc.date.issued2019-08-05
dc.identifier.citationZhang SH, Liu DH, Hu QY, Zhu JL, Wang SQ, Zhou S (2019) 'Ferulic acid ameliorates pentylenetetrazol-induced seizures by reducing neuron cell death', Epilepsy Research, 156 (106183), pp.-.en
dc.identifier.issn0920-1211
dc.identifier.pmid31404716
dc.identifier.doi10.1016/j.eplepsyres.2019.106183
dc.identifier.urihttp://hdl.handle.net/10547/623386
dc.description.abstractAbstract: To investigate the neuroprotective effect of ferulic acid (FA) in a pentylenetetrazol (PTZ)-induced seizures rat model, the seizures behaviour, spatial learning ability and memory capability of the rats were assessed. Both the antioxidation and anti-apoptosis pathways were also investigated. In this study, male Wistar rats were randomly divided into 3 groups (n = 12 in each group). For 28 days, the rats were administered saline alone (i.p. normal saline, NS group), PTZ (40 mg/kg, i.p., PTZ group) once daily to induce seizures, or FA (i.p. 60 mg/kg) 20 min before being given PTZ (40 mg/kg, i.p., FA + PTZ group) to assess the neuroprotective effect of FA. The seizures behaviour of the rats was analysed with the Racine scale. The spatial learning and memory capacity of the rats were assessed by the Morris water maze test. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured, and both in situ staining with the DNA-binding bisbenzimide Hoechst 33258 and TUNEL assays were used to assess apoptosis. Western blotting was used to further analyse the expression of Apaf-1, caspase-9, caspase-3, Bcl-2, Bid, Bax, cleaved caspase-3 and cytochrome c. The results showed that compared to the those of the PTZ group, FA pre-treatment significantly (p < 0.01) reduced the Racine scores starting at day 4, prolonged the latency of the onset of seizure at day 28, reduced the escape latency period starting at day 2, increased the frequency of crossing the platform location, increased the SOD activity, reduced the MDA content and apoptosis rate, and upregulated the Bcl-2 levels whilst downregulating the Bax, cytochrome c, Apaf-1, caspase-9, caspase-3, cleaved caspase-3 and Bid expression levels. This study demonstrated that pre-treatment with FA exerts strong neuroprotective effects by reducing seizures behaviour and by improving spatial learning ability and memory capacity. The neuroprotective effect may be a result of a reduction in neuron cell death that occurs via the antioxidative and anti-apoptotic pathways. 
dc.language.isoenen
dc.publisherElsevieren
dc.relation.urlhttps://www.sciencedirect.com/science/article/pii/S0920121119302049en
dc.rightsGreen - can archive pre-print and post-print or publisher's version/PDF
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectferulic aciden
dc.subjectepilepsyen
dc.subjectspatial learningen
dc.subjectmemory capacityen
dc.subjectapoptosisen
dc.subjectoxidative stressen
dc.subjectB120 Physiologyen
dc.titleFerulic acid ameliorates pentylenetetrazol-induced seizures by reducing neuron cell deathen
dc.typeArticleen
dc.contributor.departmentJiamusi Universityen
dc.contributor.departmentUniversity of Bedfordshireen
dc.identifier.journalEpilepsy Researchen
dc.date.updated2019-08-19T09:08:15Z
dc.description.note12 m embargo
html.description.abstractAbstract: To investigate the neuroprotective effect of ferulic acid (FA) in a pentylenetetrazol (PTZ)-induced seizures rat model, the seizures behaviour, spatial learning ability and memory capability of the rats were assessed. Both the antioxidation and anti-apoptosis pathways were also investigated. In this study, male Wistar rats were randomly divided into 3 groups (n = 12 in each group). For 28 days, the rats were administered saline alone (i.p. normal saline, NS group), PTZ (40 mg/kg, i.p., PTZ group) once daily to induce seizures, or FA (i.p. 60 mg/kg) 20 min before being given PTZ (40 mg/kg, i.p., FA + PTZ group) to assess the neuroprotective effect of FA. The seizures behaviour of the rats was analysed with the Racine scale. The spatial learning and memory capacity of the rats were assessed by the Morris water maze test. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured, and both in situ staining with the DNA-binding bisbenzimide Hoechst 33258 and TUNEL assays were used to assess apoptosis. Western blotting was used to further analyse the expression of Apaf-1, caspase-9, caspase-3, Bcl-2, Bid, Bax, cleaved caspase-3 and cytochrome c. The results showed that compared to the those of the PTZ group, FA pre-treatment significantly (p < 0.01) reduced the Racine scores starting at day 4, prolonged the latency of the onset of seizure at day 28, reduced the escape latency period starting at day 2, increased the frequency of crossing the platform location, increased the SOD activity, reduced the MDA content and apoptosis rate, and upregulated the Bcl-2 levels whilst downregulating the Bax, cytochrome c, Apaf-1, caspase-9, caspase-3, cleaved caspase-3 and Bid expression levels. This study demonstrated that pre-treatment with FA exerts strong neuroprotective effects by reducing seizures behaviour and by improving spatial learning ability and memory capacity. The neuroprotective effect may be a result of a reduction in neuron cell death that occurs via the antioxidative and anti-apoptotic pathways. 


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