Gu Xiangjin,Xu Jin,Ma Banyou,Chen Gong,Gu Peiyuan,Wei Dong,Hu Weixing.[J].Chin J Traumatol,2014,17(1):1-7. [doi]
Effect of glycyrrhizin on traumatic brain injury in ratsand its mechanism
  
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KeyWord: Glycyrrhizic acid  HMGB1 protein  Brain injuries  Neuroprotective agents
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Author NameAffiliation
Gu Xiangjin Department of Neurosurgery, Jiangning Hospital Affiliated to Nanjing Medical University, Nanjing 211100, China 
Xu Jin Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
Ma Banyou Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
Chen Gong Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
Gu Peiyuan Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
Wei Dong Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
Hu Weixing Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China 
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Abstract:
      Objective: To investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB1) in rats after traumatic brain injury(TBI). Methods: Male Sprague-Dawley rats were randomly divided into three groups: sham group, TBI group, and TBI+Gly group (n=36 per group). Rat TBI model was made by using the modified Feeney’s method. In TBI+Gly group, Gly was administered intravenously at a dosage of 10 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB1/HMGB1 receptors including toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE)/nuclear factor-κB(NF-κB) signaling pathway and inflammatory cytokines in the injured brain tissues were detected using quantitative real-time polymerase chain reaction, western blot, electrophoretic mobility shift assay and enzyme-linked immunosorbent assay. Furthermore, HMGB1, RAGE and TLR4 immunohistochemistry and apoptosis were analyzed. Results: Beam walking performance impairment and brain edema were significantly reduced in TBI+Gly group compared with TBI group; meanwhile, the over-expressions of HMGB1/HMGB1 receptors (TLR4 and RAGE)/NF-κ B DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB1, RAGE and TLR4-positive cells and apoptotic cells were respectively 58.37%±5.06%, 54.15%±4.65%, 65.50%± 4.83%, 52.02%±4.63% in TBIgroupand39.99%±4.99%,34.87%±5.02%,43.33%±4.54%, 37.84%±5.16% in TBI+Glygroup (all P<0.01compared with TBI group). Conclusion: Gly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regulationofHMGB1/HMGB1receptors (TLR4andRAGE)/NF-κBmediated inflammatory responses in the injured rat brain.
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