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 |
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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 |
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Abstract | 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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AbstractList | 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-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.RESULTSBeam 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-κB-mediated inflammatory responses in the injured rat brain. 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. 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). 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. 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). 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. 【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. 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) 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 10mg/kg 30min after TBI. At 24h 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 analyzed 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). Gly 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. Objective:To investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB 1) 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,HMGB 1/HMGB 1 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,HMGB 1,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 1/HMGB 1 receptors (TLR4 and RAGE)/NF-κB DNA-binding activity and inflammatory cytokines were inhibited.The percentages of HMGB 1,RAGE and TLR4positive 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 HMGB 1/HMGB 1 receptors (TLR4 and RAGE)/NF-κ B-mediated inflammatory responses in the injured rat brain. |
Author | Gu Xiangjin Xu Jin Ma Banyou Chen Gong Gu Peiyuan Wei Dong Hu Weixing |
AuthorAffiliation | Department of Neurosurgery, Jiangning Hospital Affili- ated to Nanjing Medical University, Nanjing 211100, China Department of Neurosurgery, the First Affiliated Hospi- tal of Nanjing Medical University, Nanjing 210029, China |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24506915$$D View this record in MEDLINE/PubMed |
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Copyright | 2014 Daping hospital and the Research Institute of Surgery of the Third Military Medical University Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
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Keywords | Glycyrrhizic acid Neuroprotective agents HMGB1 protein Brain injuries |
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Notes | 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 |
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PublicationYear | 2014 |
Publisher | Elsevier B.V 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 |
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Snippet | 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... 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... OBJECTIVETo investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB1) in rats... Objective:To investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB 1) in rats... 【Abstract】Objective: To investigate the neuroprotective effects of glycyrrhizin (Gly) as well as its effect on expression of high-mobility group box 1 (HMGB1)... |
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SubjectTerms | Animals Brain injuries Brain Injuries - drug therapy DNA结合活性 Glycyrrhizic acid Glycyrrhizic Acid - pharmacology Glycyrrhizic Acid - therapeutic use HMGB1 protein HMGB1 Protein - metabolism Male Neuroprotective agents Neuroprotective Agents - therapeutic use RAGE Rats Rats, Sprague-Dawley SD大鼠 Toll样受体4 创伤性脑损伤 甘草甜素 神经保护作用 脑组织含水量 |
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Title | Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism |
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