title: Glycyrrhizin protects spinal cord and reduces inflammation in spinal cord ischemia-reperfusion injury.
abstract: OBJECTIVE
  Inflammation, which is detrimental to the neurologic defect after ischemia-reperfusion, provides a potential target for therapeutic approach for spinal cord ischemia-reperfusion injury. High mobility group box 1 (HMGB-1) was recently discovered to be a crucial cytokine that mediates the response to infection, injury and inflammation. The present study aimed to gain a deep insight into the neuroprotective effect of glycyrrhizin in the process of ischemia and reperfusion injury in spinal cord of mice.
  
  
  METHODS
  Spinal cord ischemia was induced in male C57BL/6 mice by occlusion of the thoracic aorta. The experimental groups (n = 6 per group) included sham operation, control (receiving phosphate buffered saline (PBS)) and glycyrrhizin (10 mg/kg, when cross-clamped). Neurologic function was assessed by the motor function score of the hind limbs at 72 hours after reperfusion. Histologic changes were studied using hematoxylin and eosin staining. Expression changes of inflammatory cytokines or their receptors at messenger RNA level or protein level were determined by real-time transcription polymerase chain reaction or enzyme-linked immunosorbent assay at different time points post reperfusion. Nuclear factor κB (NF-κB) activity was examined with Western blotting.
  
  
  RESULTS
  Compared with the control group, the glycyrrhizin group showed significantly improved neurologic outcome, reduced apoptosis of motoneurons of spinal anterior horn, decreased the activation of NF-κB and subsequent inflammatory cytokines expression [tumor necrosis factor (TNF) and interleukin 1β (IL-1β)], and alleviated neutrophil infiltration in ischemic spinal cord. HMGB-1 treatment also reduced the expressions of itself.
  
  
  CONCLUSIONS
  Treatment with glycyrrhizin exerted a neuroprotective effect against spinal cord ischemia-reperfusion injury. The anti-inflammatory effect was believed to be one of the contributing mechanisms. Our findings provided experimental and therapeutic options for the treatment of spinal cord ischemia-reperfusion injury.
authors.affiliation: Department of Orthopedics, Shanghai Changzheng Hospital , Shanghai , China.
authors.forename: Bin
authors.initials: B
authors.lastname: Ni
authors.forename: Zhenyu
authors.initials: Z
authors.lastname: Cao
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000818:Animals; D019695:Glycyrrhizic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D020760:Spinal Cord Ischemia / Q000378:metabolism / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis
chemical_list: D018836:Inflammation Mediators; D016328:NF-kappa B; D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D019695:Glycyrrhizic Acid