Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Dexmedetomidine relieves inflammatory response in rats with acute spinal cord injury through IKK/NF-κB signaling pathway

Haijuan Zhu, Jinbao Wang , Lihua Huang

Department of Anesthesiology, The 980th Hospital of PLA Joint Logistics Support Force, Shijiazhuang 050082, Hebei Province, China;

For correspondence:- Jinbao Wang Email: w15830185510@163.com

Accepted: 2 March 2022 Published: 31 March 2022

Citation: Zhu H, Wang J, Huang L. Dexmedetomidine relieves inflammatory response in rats with acute spinal cord injury through IKK/NF-κB signaling pathway. Trop J Pharm Res 2022; 21(3):543-548 doi: 10.4314/tjpr.v21i3.13

© 2022 The authors.
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Abstract

Purpose: To examine the effect of dexmedetomidine (DEX) on inflammatory response in spinal cord damage, and involvement of IKK/NF-κB signaling pathway in the process.

Methods: Sixty healthy male Wistar rats were selected and randomly divided into sham, control, IKK inhibition, and DEX groups. Rat hind limb motor function in each group at 1, 24 and 48 h after surgery was determined using Basso Beattie Bresnahan (BBB) method, while Western blot assay was used to evaluate the protein expression levels of IL-1β, IKK and NF-κB in spinal cord tissue.

Results: In DEX rat group, neuromotor function at 24 and 48 h, and protein expression level of IL-1β in spinal cord tissue significantly decreased, relative to IKK inhibition group (p < 0.05). There were higher protein expressions of IKK and NF-κB in IKK inhibition and DEX groups than in sham rats, but were lower than the corresponding values for model group (p < 0.05). However, these proteins were significantly downregulated in DEX group, relative to the IKK inhibition rats (p < 0.05).

Conclusion: DEX mitigates inflammatory response in rats with acute spinal cord injury via IKK/NF-κB signaling pathway. This provides some ideas for research and development of other drugs for the treatment of acute spinal cord injury.

Keywords: Dexmedetomidine, Acute spinal cord injury, Nuclear factor kappa B, Inflammatory response