No abstract

Whole body vibration (WBV), as a form of physical stimulation through mechanical vibration, has been proved to have neuroprotective effects on a variety of central nervous system (CNS) diseases. However, whether WBV plays a neuroprotective role in early brain injury (EBI) after subarachnoid hemorrhage (SAH) has not been well demonstrated. Herein, we focused on investigating the potential mechanism of the therapeutic effects of WBV on SAH-induced mice. The endovascular perforation was performed to induce SAH in C57BL/6J male mice. The mice were exposed to WBV twice a day at a frequency of 30 Hz for 20 days. The curative actions of WBV were assessed using the modified Garcia scale and the beam balance scoring system, along with measuring brain water content 24 h after SAH induction. TUNEL staining was performed to observe the apoptotic cells. Immunofluorescence staining was used to evaluate the expression of astrocytes and microglia in mice's cerebral cortex. Additionally, the ELISA assay was performed to detect inflammatory cytokines, such as IL-10, IL-18, and IL-1β. Western blot was conducted to explore the expression analysis of apoptosis-associated proteins (cleaved Caspase-3). Morris Water Maze (MWM) test and rotarod test were used to evaluate the long-term neurological function of mice. Nissl staining was used to evaluate the loss of neurons in the hippocampus of mice. Our study illustrated that WBV can reduce brain water content without significantly affecting the weight of mice. Also, the TUNEL-positive cell counts of the cerebral cortex of mice in the SAH+WBV group were significantly reduced compared with that in the SAH group. The protein level of cleaved Caspase-3 in the SAH+WBV group was also decreased than that in the SAH group. Immunofluorescence staining showed that WBV suppressed the high expression of GFAP and Iba-1 caused by SAH. MWM assay and rotarod test revealed that the long-term neurological dysfunction of mice following SAH was attenuated by WBV treatment compared with SAH-induced mice, which may be closely related to the low level of neuronal loss in the hippocampal regions. Our research demonstrated that WBV treatment can reduce EBI and neuroinflammation and improve the long-term neurological dysfunction of mice after SAH, which provides a new possibility for clinical treatment of SAH in the future.