Effects of minocycline on motor function recovery and expression of glial fibrillary acidic protein and brain-derived neurotrophic factor after spinal cord injury in rats.

Abstract

Study explore the effects of minocycline on the expression of glial fibrillary acidic protein and brain-derived neurotrophic factor after spinal cord injury and its possible mechanism of action. The model of acute spinal cord injury was established by Allen's method. The rats in each group were assessed with Basso Beattie Bresnahan score of hindlimb motor function and inclined plate test score. Serum malondialdehyde and superoxide dismutase, glial fibrillary acidic protein and brain-derived neurotrophic factor in spinal cord were compared. Basso Beattie Bresnahan scores, Tiltboard experiment max angles, and Serum superoxide dismutase activity of the minocycline group were higher than those of the model group after surgery (P < 0.05). Serum malondialdehyde content, and expression of the minocycline group was lower than that of the model group (P < 0.05), and brain-derived neurotrophic factorexpression of minocycline group was significantly higher in the model group after surgery (P < 0.05). Minocycline can promote the recovery of motor function after spinal cord injury in rats. The mechanism of action may be that it inhibits local free radical generation, reduces lipid peroxidation and glial fibrillary acidic protein expression in spinal cord tissue after spinal cord injury, and promotes the synthesis of endogenous brain-derived neurotrophic factor, thus improving the microenvironment of spinal cord regeneration after spinal cord injury in rats.