Neuroprotective effect and mechanism of idebenone on hippocampal damage induced by epileptic seizure

Shan QIAO, Yong-xin SU, Ran-ran ZHANG, Yu-jiao WU, Ke-mo WANG, Xue-wu LIU

Abstract


Objective To investigate the protective effect of idebenone (IDBN) on hippocampal neuron injury in epileptic rats and its mechanism. Methods Forty-eight Wistar rats were randomly divided into normal control group, IDBN prevention group (prevention group), epilepsy group, IDBN 25, 50 and 100 mg groups. Behavioral changes of rats in different treatment groups before and after treatment with IDBN were observed. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in hippocampal were detected. The ultrastructural changes of hippocampal neurons and mitochondria were observed. Results The expression levels of SOD, GSH-Px and MDA in different treatment groups were significantly different (P = 0.000, for all). The activity of SOD and GSH-Px was the highest and the content of MDA was the lowest in IDBN 100 mg group. The activity of SOD and GSH-Px in IDBN 100 mg group were higher than those in epilepsy group (P = 0.000, 0.000), IDBN 25 mg group (P = 0.000, 0.000) and 50 mg group (P = 0.004, 0.005), while the content of MDA was lower than that in epilepsy group (P = 0.000), IDBN 25 mg group (P = 0.000) and 50 mg group (P = 0.002). Compared with normal control group and prevention group, hippocampal neurons in epilepsy group showed different degrees of damage, which was relieved after treatment with IDBN and gradually decreased with the increase of dose. In epilepsy group, the mitochondrial structure of hippocampal neurons was damaged obviously, with deformation and swelling, and some mitochondria were vacuolated. After treatment with IDBN, the damage was relieved, and the 100 mg group had the least damage. Conclusions IDBN can protect hippocampal neuron structure and function by inhibiting oxidative stress injury in epileptic rats.

 

doi:10.3969/j.issn.1672⁃6731.2022.07.008


Keywords


Benzoquinones; Epilepsy; Hippocampus; Apoptosis; Superoxide dismutase; Glutathione peroxidase; Malondialdehyde; Disease models, animal

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