title: Protective effects of quercetin against status epilepticus induced hippocampal neuronal injury in rats: involvement of X-linked inhibitor of apoptosis protein.
abstract: Epilepsy is a common neurological disorder affecting people worldwide, and the recurrent spontaneous seizures are often seen post status epilepticus. Apoptosis and necrosis are two forms of neuronal death in post status epilepticus hippocampus, and the former has been widely studied and believed to be a major factor contributing to formation of abnormal excitatory circuit leading to refractory epileptic events. Thus, the need for development of new anti-epileptic agents remains urgent. Quercetin, a plant-derived bioflavonoid, is reported to have neuroprotective effects in neurological disease. We investigated protective effects of quercetin on status epilepticus induced hippocampal neuronal injuries in rats and focused on two major proteins, the X-linked inhibitor of apoptosis protein, a key member of the inhibitor of apoptosis protein family, and the caspase-3 protein, a common effector for the execution-phase of cell signaling apoptotic pathways. The number of apoptotic and surviving neurons were also counted in this study. We found expression alterations of X-linked inhibitor of apoptosis protein and caspase-3 protein in post status epilepticus hippocampus, along with an alteration in the number of apoptotic and surviving neurons. Furthermore, quercetin treatment in rats undergoing status epilepticus led to an interventional effect on expression of X-linked inhibitor of apoptosis protein and the caspase-3 protein, with a corresponding positive change on the number of hippocampal apoptotic and surviving neurons. Together, the study suggests neuroprotective effects of quercetin on hippocampal injury post status epilepticus and the effects may be associated with regulation of the X-linked inhibitor of apoptosis protein and the caspase-3 protein, which can be a decisive factor for apoptosis and survival of neurons in hippocampus.
authors.affiliation: Department of Neurology, Xiangya Hospital, Central South University, P. R. China.
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Shu-Yu
authors.initials: SY
authors.lastname: Li
authors.forename: Bo
authors.initials: B
authors.lastname: Xiao
authors.forename: Fang-fang
authors.initials: FF
authors.lastname: Bi
authors.forename: Xiao-Qin
authors.initials: XQ
authors.lastname: Lu
authors.forename: Xiao-Mei
authors.initials: XM
authors.lastname: Wu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D051636:X-Linked Inhibitor of Apoptosis Protein / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; D051636:X-Linked Inhibitor of Apoptosis Protein; D011794:Quercetin; C505410:Casp3 protein, rat; D053148:Caspase 3