| 摘要 |
[Objectives] To investigate the effect of low-intensity focused ultrasound (LIFU) on rats with spinal cord injury (SCI) by examining the expression of calcineurin (CaN) and nuclear factor of activated T-cells (NFAT) in the injured spinal cord region following LIFU intervention. [Methods] Twenty-four specific pathogen-free (SPF) female Wistar rats, aged 7-8 weeks (160-180 g), were selected. Six rats were randomly assigned to the sham-operated group (SHAM), undergoing laminectomy only without spinal cord injury. Spinal cord injury models were established in the remaining rats using a modified Allen’s weight-drop method at the T10 thoracic vertebral level. The 18 rats with successful modeling were then randomly divided into the spinal cord injury model group (SCI group), LIFU treatment group 1 (T1 group), and LIFU treatment group 2 (T2 group), with six rats in each group. LIFU treatment (for T1 and T2 groups) commenced on day 4 after injury, administered once daily for 20 min per session, for a total of 11 consecutive days. Tissues were harvested on day 14. Changes in CaN and NFAT4 mRNA expression were assessed using quantitative polymerase chain reaction (qPCR). Changes in CaN and NFAT4 protein expression were evaluated by Western blot analysis. [Results] qPCR analysis revealed that compared to the SHAM group, mRNA expression levels of both CaN and NFAT4 were decreased in the SCI group; compared to the SCI group, mRNA expression levels of CaN and NFAT4 were increased in both the T1 and T2 groups; furthermore, compared to the T1 group, mRNA expression levels of CaN and NFAT4 were higher in the T2 group. Western Blot analysis showed that compared to the SHAM group, protein expression levels of both CaN and NFAT4 were downregulated in the SCI group; compared to the SCI group, protein expression levels of CaN and NFAT4 were increased in both the T1 and T2 groups; moreover, compared to the T1 group, protein expression levels of CaN and NFAT4 were higher in the T2 group. [Conclusions] LIFU may contribute to functional recovery in SCI rats by modulating the expression levels of CaN and NFAT4. |