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Objective To investigate the long⁃term stability of syringomyelia (SM) rat model constructed by epidural compression. Methods A total of 35 Sprague⁃Danley (SD) rats were randomly divided into sham surgery group (n=9), short⁃term group (n=6) and long⁃term group (n=20). The central spinal canal was blocked by epidural compression to induce SM in rats. Basso⁃Beattie⁃Bresnahan score (BBB) was used to evaluate lower limb motor function before surgery and at 3, 6, 9 and 12 months after surgery. The morphological changes of SM were evaluated by MRI and HE staining at 2 and 12 months after surgery. Results At 2 and 12 months after surgery, MRI showed 80% (16/20) and 85% (17/20) rats in long⁃term group had SM. Compared with 2 months after surgery, the ratio of the maximum cavity diameter to the diameter of spinal cord plane (Z=⁃3.518, P=0.000) and the ratio of the maximum cavity area to the area of spinal cord plane (Z=⁃3.464, P=0.001) increased in long⁃term group at 12 months after surgery. At 2 and 12 months after surgery, the morphology of the spinal cord was normal and there was no cavity in sham surgery group, while the spinal cord cavity was observed in the short⁃term group at 2 months after surgery. At 12 months after surgery, the cavity area of the long⁃term group was not only larger than that of the short⁃term group, but also involved more vertebral segments. There was no significant difference in BBB score between sham surgery group and long⁃term group at different time points before and after surgery (P＞0.05, for all). Conclusions The rat model of SM constructed by epidural compression has high positive rate, good long⁃term stability, and does not affect the motor function of rats.

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.