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 inChinese journal of traumatology Vol. 17; no. 1; pp. 1 - 7
Main Authors Xiangjin, Gu, Jin, Xu, Banyou, Ma, Gong, Chen, Peiyuan, Gu, Dong, Wei, Weixing, Hu
Format Journal Article
LanguageEnglish
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
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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.
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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CitedBy_id crossref_primary_10_3389_fphar_2021_611610
crossref_primary_10_3389_fphar_2021_822154
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DocumentTitleAlternate Effect of glycyrrhizin on traumatic brain injury in rats and its mechanism
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Keywords Glycyrrhizic acid
Neuroprotective agents
HMGB1 protein
Brain injuries
Language English
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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.
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PublicationTitle Chinese journal of traumatology
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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
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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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https://www.ncbi.nlm.nih.gov/pubmed/24506915
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https://d.wanfangdata.com.cn/periodical/zhcszz-e201401001
https://doaj.org/article/5f09fa2716fd49b7be2d2b5b273d3c7e
Volume 17
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