The Influence of Mild Hypothermia Plus Methylprednisolone on Nerve Function and Apoptosis by Inhibiting P38AMPK/Smad2 Pathway
The Influence of Mild Hypothermia Plus Methylprednisolone on Nerve Function and Apoptosis by Inhibiting P38AMPK/Smad2 Pathway
Lihang Wang, Qiling Chen, Tingsheng Lu, Shudan Yao, Xingwei Pu and Chunshan Luo*
ABSTRACT
The main aim of this study was to explore the mechanism of mild hypothermia (MH) plus methylprednisolone (MPS) was in spinal cord injury (SCI) therapy. Application of modified Allen’s method was for injury of the spinal cord (T10) in rats and treated SCI was with MH or/and MPS immediately. Conduction of Basso-Beattie-Bresnahan (BBB) scores was on all rats at different time points after surgery. Subsequently harvest of the serum and the spinal cord tissues was behind euthanasia of rats. Detection of biochemical indicators, observation of cell apoptosis, and determination of Bax, Bcl-2, p38 MAPK and Smad2 were clarified. We found that MH and MH+MPS could effectively reduce apoptotic cells, dramatically minify TNF-α, IL-6, IL-8, MDA and Bax contents (P < 0.01) and elevate GSH-Px and Bcl-2 level (P < 0.01). Additionally, the P38AMPK/Smad2 pathway proteins (phosphorylated p -P38MAPK and Samd2) were notably higher in the model versus the control and the sham, while MH and MH+MPS could patently down-regulate p-P38MAPK and Samd2 protein levels. To conclude, MH+MPS is available to refrain the activation of P38AMPK/Smad2 signal, hence repressing cell apoptosis after SCI, reducing secondary SCI, and benefiting the recovery of nerve function.
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