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.