| Summary: | 【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-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).
Conclusion: Gly can reduce secondary brain injury and improve outcomes in rat following TBI by down-regulation of HMGB1/HMGB1 receptors (TLR4 and RAGE)/NF-κB -
mediated inflammatory responses in the injured rat brain.
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