Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism
Objective: To investigate the neuropro- tective 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...
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Published in | Chinese journal of traumatology Vol. 17; no. 1; pp. 1 - 7 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
China
Elsevier B.V
01.02.2014
Department of Neurosurgery, Jiangning Hospital Affiliated to Nanjing Medical University, Nanjing 211100, China%Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Objective: To investigate the neuropro- tective 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 l0 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB 1/HMGB 1 receptors including toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE)/nuclear fac- tor-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, HMGB l, 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 HMGB 1PHMGB 1 receptors (TLR4 and RAGE)/NF- κB DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB 1, 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-regula- tion of HMGB 1/HMGB 1 receptors (TLR4 and RAGE)/NF- κB - mediated inflammatory responses in the injured rat brain. |
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Bibliography: | Glycyrrhizic acid; HMGBl protein; Braininjuries; Neuroprotective agents Objective: To investigate the neuropro- tective 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 l0 mg/kg 30 min after TBI. At 24 h after TBI, motor function and brain water content were evaluated. Meanwhile, HMGB 1/HMGB 1 receptors including toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE)/nuclear fac- tor-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, HMGB l, 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 HMGB 1PHMGB 1 receptors (TLR4 and RAGE)/NF- κB DNA-binding activity and inflammatory cytokines were inhibited. The percentages of HMGB 1, 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-regula- tion of HMGB 1/HMGB 1 receptors (TLR4 and RAGE)/NF- κB - mediated inflammatory responses in the injured rat brain. 50-1115/R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1008-1275 |
DOI: | 10.3760/cma.j.issn.1008-1275.2014.01.001 |