Chinese Journal of Tissue Engineering Research ›› 2013, Vol. 17 ›› Issue (53): 9189-9195.doi: 10.3969/j.issn.2095-4344.2013.53.015

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Dexmedetomidine inhibits renal ischemia/reperfusion-induced inflammatory reaction

Chen Ke-yan, Zhang Yi-nan, Diao Yu-gang, Zhou Jin, Zhang Tie-zheng   

  1. Department of Anaesthesiology, General Hospital of Shenyang Military Region, Shenyang  110016, Liaoning Province, China
  • Revised:2013-09-16 Online:2013-12-31 Published:2013-12-31
  • Contact: Zhang Tie-zheng, Master, Chief physician, Department of Anaesthesiology, General Hospital of Shenyang Military Region, Shenyang 110016, Liaoning Province, China tzzhang@hotmail.com
  • About author:Chen Ke-yan☆, M.D., Department of Anaesthesiology, General Hospital of Shenyang Military Region, Shenyang 110016, Liaoning Province, China chenkeyan888@163.com
  • Supported by:

    a grant from Liaoning Provincial Science and Technology Program, No. 2012225006*

Abstract:

BACKGROUND: Previous studies addressing the prevention and treatment of ischemia/reperfusion kidney damage show that, some drugs could activate or inhibit the body to protect kidney tissue, which is of great significance in renal transplantation and graft functional recovery.
OBJECTIVE: To explore the influence of dexmedetomidine on expressions of inflammatory factors and C-X-C chemokine receptor type 4 in rat with renal ischemia/reperfusion.
METHODS: Forty rats were randomly divided into four equal groups: sham group, ischemia/reperfusion group, dexmedetomidine preconditioning group and dexmedetomidine post-treatment group. Except the sham group, the right kidney was removed and the left kidney was subject to ischemia for 45 minutes and reperfusion for 60 minutes, thus establishing renal ischemia/reperfusion models in other three groups. As for preconditioning group, the rat femoral vein was punctured and transfused with 1 μg/kg dexmedetomidine for 10 minutes, followed by infusing 0.5 μg/kg dexmedetomidine for 30 minutes until ischemia occurred. As for posttreatment group, the rats were infused with 0.5 μg/kg dexmedetomidine for 30 minutes after reperfusion.
RESULTS AND CONCLUSION: Serious kidney injury, obvious inflammation, tubular dilatation, and glomerulonephritis were found in rats with renal ischemia/reperfusion. The serum interleukin-1β and tumor necrosis factor-α levels in ischemia/reperfusion, dexmedetomidine preconditioning and dexmedetomidine post-treatment groups were increased significantly (P < 0.05). The expression of serum and renal C-X-C chemokine receptor type 4 was also increased (P < 0.05). Dexmedetomidine preconditioning or post-treatment significantly decreased serum interleukin-1β and tumor necrosis factor-α levels in rats with renal ischemia/reperfusion (P < 0.05). The same decline was observed in content of serum and renal C-X-C chemokine receptor type 4 (P < 0.05). Experimental findings indicate that renal ischemia/reperfusion can cause renal injury which is characterized by inflammatory reaction. Dexmedetomidine can reduce inflammatory reactions and attenuate C-X-C chemokine receptor type 4 expression to protect the kidney.



中国组织工程研究
杂志出版内容重点:肾移植肝移植移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植组织工程


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Key words: reperfusion injury, systemic inflammatory response syndrome, α-adrenergic agonist, renal transplantation

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