Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism

ObjectiveTo 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)MethodsMale 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- κ B(NF- κ B) 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 analyzedResultsBeam 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-κB 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 TBI group and 39.99% ± 4.99%, 34.87% ± 5.02%, 43.33% ± 4.54%, 37.84% ± 5.16% in TBI + Gly group (all P < 0.01 compared with TBI group).ConclusionGly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regulation of HMGB1/HMGB1 receptors (TLR4 and RAGE)/NF-κ B-mediated inflammatory responses in the injured rat brain.