To evaluate the effect of p38
pathway on spinal cord injury
(SCI), a rat
model of SCI was performed.
We determined the effect of p38
on SCI and SCI related inflammation
, and autophagy
Summary of Background Data.
SCI is a severe clinical problem worldwide. It is difficult to prevent cell necroptosis and promote the survival of residual neurons after SCI. p38
, a class of mitogen-activated protein kinases, its effect on SCI and SCI related inflammation
, and autophagy
have not been studied very well.
The rats were randomly divided into the following four groups: the sham-operated (sham) group, the SCI group, the SCI + vehicle group, and the SCI + SB203580
(10 mg/kg) group. The p38
was administered by oral (10 mg/kg/d) gavage once per day for 14 days. Neurological recovery
was assessed using the Basso, Beattie, and Bresnahan locomotion rating scale. Apoptosis
, and inflammation
related proteins were measured by enzyme-linked immunosorbent assay kits or western blotting.
Our results showed that p38
was upregulated after SCI from day 3, which was paralleled with the levels of its proteins ATF-2, suggesting an increase in p38
activity. Our results showed administration of SB203580
attenuated histopathology and promoted locomotion recovery in rats after SCI. SB203580
administration significantly inhibited inflammatory cytokines
levels as well as the inflammation
signaling pathway. SB203580
administration also modulated the apoptosis
Our findings suggest that p38
treatment alleviates secondary SCI by inhibiting inflammation
, thereby promoting neurological and locomoter functional recovery, thus suggest the important role of p38
in neuronal protection
Level of Evidence: N/A