Abstract
Study Design: This study investigated the outcome of epigallocatechin (EGCG) against edema after spinal cord injury (SCI). Objective: To perform the evidence correlation of EGCG with p38MAPK\NF-κB\AQP4 signaling pathway, also explore the effect of EGCG on edema after SCI, and clarify the possible mechanism of the EGCG reducing the edema after SCI. Summary of background data: Although some studies show that EGCG have a protective effect on nerve cells, there are few documents covering the relation between EGCG and SCI. On the basis of confirming significant inhibition of EGCG against edema after SCI, our research group intended to take the lead in further demonstrating the mechanism of anti-edema of EGCG against SCI. Methods: 160 rats were randomly divided into sham - surgery, SCI, EGCG and specific p38MAPK inhibitor SB203580 treatment groups, every group contained 40 rats. Acute SCI models were established in rats by vascular clip method. We used sensitive ELISA to examine the level of TNF-α and IL-1β, Western blot to examine the expression of p38MAPK/NF- κB/AQP4 signaling pathway related protein, the change of water content in spinal cordto evaluate the effect of EGCG against edema after SCI therapy. Results: Both EGCG and SB203580 groups could significantly reduce the releasing of TNF-α and IL-1β (P<0.05), while EGCG had a better effect (P<0.05), thus EGCG could significantly inhibit the phosphorylation status of p38MAPK reduce the expression of NF-κB p65 and AQP4 (P<0.05), and decrease the water content after SCI (P<0.05), similar to SB203580. Conclusion: The experimental findings indicate that EGCG can protect secondary SCI by potential mechanism of regulating p38MAPK\NF -κB\AQP4 signaling pathwayand thus reduce edema after SCI.
Highlights
Spinal cord injury (SCI) is a serious health problem with high care costs and involves primary and secondary mechanisms of injury
Both EGCG and SB203580 groups could significantly reduce the releasing of TNF-α and IL-1β (P
The experimental findings indicate that EGCG can protect secondary SCI by potential mechanism of regulating p38MAPK\NF -κB\AQP4 signaling pathway and reduce edema after SCI
Summary
Spinal cord injury (SCI) is a serious health problem with high care costs and involves primary and secondary mechanisms of injury. SCI destroys the local nerve tissues at the injured site by mechanical trauma. The secondary injury can destroy neighbouring nerve tissue that is not involved in the primary injury [1]. It is the key to curing SCI, the specific link that is susceptible to therapy. This is especially important since drug treatment is an essential part of SCI treatment and recovery and can affect the prognosis. The only drug effective for the treatment of acute spinal cord injury is methylprednisolone [3], even this drug is receiving scepticism from orthopaedics specialists due to its narrow application window and various complications [4]. To find a safe and effective drug which can be long-term used has been a hot and difficult problem for many orthopaedic experts
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