Triptolide Promotes the Repair of Spinal Cord Injury by Inhibiting Autophagy in Rats Models

Using rat models with spinal cord injuries, we examined the efficacy of Triptolide (TP) on motor function through the inhibition of autophagy. 60 rats were used and divided into three groups randomly: SHAM, DMSO and TP groups. The SHAM group (n = 20) underwent a surgical procedure to open the lamina without damage to the spinal cord. In the DMSO-group (n = 20), the right-hemisected model of the spinal cord was formed followed by treatment with DMSO without TP. In the TP group (n = 20), the right-hemisected model of the spinal cord was formed, followed by the treatment with DMSO and TP. Bright field microscopy results displayed an obvious reduction in the cavity area of the TP group when compared to the DMSO group. There was also a significant increase in BBB scores and motor function. The immunofluorescence and western blotting analyses used to in the examination of the expression of the Microtubule-associated protein 2 (MAP-2) in the nerve cells found the treatment with TP to significantly increase the expression of MAP-2. More so, the immunofluorescence and western blotting analyses demonstrated the treatment with TP significantly decreased both the light chain 3 (hereafter: LC3's) expression and the Beclin-1's expression. These results substantiate that treatment with Triptolide can improve recovery from spinal cord injury through the inhibition of autophagy signaling pathways.