Effects of Whole-Body Vibration Training on Neurological Function and Ferroptosis in A Rat Model with Cerebral Ischemia-Reperfusion Injury

ObjectiveTo observe the effects of whole-body vibration training on the neurological function and ferroptosis in rat model with cerebral ischemia-reperfusion injury (CIRI), and to explore the mechanism by which whole-body vibration training ameliorates CIRI.MethodsForty SPF-grade male Sprague-Dawley (SD) rats were randomly divided into sham operation group (<italic>n</italic>=10) and model group (<italic>n</italic>=30) according to the random number table method. The model group rats were sujected to the modified Zea-Longa wire embolization method to create a CIRI model. The dynamic monitoring of brain blood flow changes before model preparation, during wire embolization insertion, and after wire embolization removal was conducted using the laser speckle blood flow imaging system to confirm the manifestations of cerebral ischemia-reperfusion. The Zea-Longa neurological deficit score was used to evaluate whether the model was successfully established. Twenty rats with successful modeling were randomly selected and randomly divided into model group and whole-body vibration training group according to the random number table method, with 10 rats in each group. The rats in the whole-body vibration training group received whole-body vibration training with a frequency of 20 Hz starting from the second day after the model establishment. The training lasted for 15 minutes each time, twice a day, and was conducted continuously for seven days. The rats in the sham operation group and the model group received no intervention. After the intervention, the Zea-Longa neurological deficit score was assessed. 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to detect the cerebral infarction area. Hematoxylin-eosin (HE) staining and Nissl staining were employed to observe pathological changes in the cerebral infarction area. Enzyme-linked immunosorbent assay (ELISA) was utilized to measure the levels of malondialdehyde (MDA), glutathione (GSH), and ferrous ions (Fe²⁺) in the cerebral infarction area. Immunofluorescence staining was applied to detect the protein expression levels of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) in the cerebral infarction area.ResultsCompared with the sham operation group, the neurological function deficit score in the model group was higher (<italic>P</italic>&lt;0.05). Compared with the model group, the neurological function deficit score in the whole-body vibration training group was lower (<italic>P</italic>&lt;0.05). Compared with the sham operation group, the percentage of cerebral infarction area in the model group was higher (<italic>P</italic>&lt;0.05). Compared with the model group, the percentage of cerebral infarction area in the whole-body vibration training group was lower (<italic>P</italic>&lt;0.05). In the model group, pathological changes in the cerebral infarction area were significant, with a reduced number of Nissl bodies, lighter staining, and scattered distribution. In the whole-body vibration training group, the pathological changes in the cerebral infarction area were milder compared to the model group, with an increased number of Nissl bodies and more uniform staining compared to the model group. Compared with the sham operation group, the levels of MDA and Fe²⁺ content in the cerebral infarction area of the model group were higher (<italic>P</italic>&lt;0.05), and the level of GSH content was lower (<italic>P</italic>&lt;0.05). Compared with the model group, the levels of MDA and Fe²⁺ content in the cerebral infarction area of the whole-body vibration training group were lower (<italic>P</italic>&lt;0.05), and the level of GSH content was higher (<italic>P</italic>&lt;0.05). Compared with the sham operation group, the fluorescence intensities of GPX4 and SLC7A11 in the left cerebral infarction area of the model group were lower (<italic>P</italic>&lt;0.05). Compared with the model group, the fluorescence intensities of GPX4 and SLC7A11 in the left cerebral infarction area of the whole-body vibration training group were higher (<italic>P</italic>&lt;0.05).ConclusionWhole-body vibration training can effectively improve the neurological function of CIRI rats and alleviate the pathological damage of neurons. The underlying mechanism may be related to the regulation of ferroptosis.