热休克蛋白70对小鼠颅脑创伤相关急性胃黏膜病变的保护作用
目的 探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法 40只成年雄性小鼠,随机分为假手术组（A组）、模型组（B组）、模型组＋GGA组（C组）、模型组＋生理盐水对照组（D组）。模型制作采用Feeney改良方法制成颅脑创伤急性胃黏膜病变模型;C组同时给予HSP70诱导剂GGA（geranylgeranylacetone,800mg/kg）灌胃。分别应用免疫组织化学法、TUNEL法检测小鼠脑组织及胃黏膜内HSP70的表达和细胞凋亡。结果 B组小鼠脑组织挫伤及胃黏膜损伤范围大于A、C组（P〈0.05）。B组小鼠脑组织及胃黏膜内HSP70的表达均有不同程度的升高,...
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| Published in | 西安交通大学学报（医学版） Vol. 37; no. 4; pp. 547 - 550 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | Chinese |
| Published |
兰州大学第二医院神经外科,甘肃兰州,730030
2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1671-8259 |
| DOI | 10.7652/jdyxb201604015 |
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| Abstract | 目的 探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法 40只成年雄性小鼠,随机分为假手术组（A组）、模型组（B组）、模型组＋GGA组（C组）、模型组＋生理盐水对照组（D组）。模型制作采用Feeney改良方法制成颅脑创伤急性胃黏膜病变模型;C组同时给予HSP70诱导剂GGA（geranylgeranylacetone,800mg/kg）灌胃。分别应用免疫组织化学法、TUNEL法检测小鼠脑组织及胃黏膜内HSP70的表达和细胞凋亡。结果 B组小鼠脑组织挫伤及胃黏膜损伤范围大于A、C组（P〈0.05）。B组小鼠脑组织及胃黏膜内HSP70的表达均有不同程度的升高,高于A组（P〈0.05）;B、D组脑组织和胃黏膜内细胞凋亡最明显,明显高于A、C组（P〈0.05）;经GGA灌胃后HSP70蛋白表达明显升高,而细胞凋亡指数明显降低,C组的HSP70表达高于B、D组,而细胞凋亡指数低于B、D组（P〈0.05）。结论 GGA灌胃后能够诱导HSP70在脑组织和胃黏膜内的表达;抑制细胞凋亡途径是HSP70保护脑组织和胃黏膜的机制之一;GGA可以用于颅脑创伤急性胃黏膜病变的预防和治疗。 |
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| AbstractList | R641; 目的：探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法40只成年雄性小鼠，随机分为假手术组（A组）、模型组（B组）、模型组＋ GGA组（C组）、模型组＋生理盐水对照组（D组）。模型制作采用Feeney改良方法制成颅脑创伤急性胃黏膜病变模型；C组同时给予 HSP70诱导剂GGA （geranylgerany‐lacetone ，800 mg／kg）灌胃。分别应用免疫组织化学法、TUNEL法检测小鼠脑组织及胃黏膜内 HSP70的表达和细胞凋亡。结果 B组小鼠脑组织挫伤及胃黏膜损伤范围大于A、C组（P＜0．05）。B组小鼠脑组织及胃黏膜内 HSP70的表达均有不同程度的升高，高于A组（P＜0．05）；B、D组脑组织和胃黏膜内细胞凋亡最明显，明显高于A、C组（P＜0．05）；经GGA灌胃后HSP70蛋白表达明显升高，而细胞凋亡指数明显降低，C组的 HSP70表达高于B、D组，而细胞凋亡指数低于B、D组（P＜0．05）。结论 GGA灌胃后能够诱导 HSP70在脑组织和胃黏膜内的表达；抑制细胞凋亡途径是 HSP70保护脑组织和胃黏膜的机制之一；GGA可以用于颅脑创伤急性胃黏膜病变的预防和治疗。 目的 探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法 40只成年雄性小鼠,随机分为假手术组（A组）、模型组（B组）、模型组＋GGA组（C组）、模型组＋生理盐水对照组（D组）。模型制作采用Feeney改良方法制成颅脑创伤急性胃黏膜病变模型;C组同时给予HSP70诱导剂GGA（geranylgeranylacetone,800mg/kg）灌胃。分别应用免疫组织化学法、TUNEL法检测小鼠脑组织及胃黏膜内HSP70的表达和细胞凋亡。结果 B组小鼠脑组织挫伤及胃黏膜损伤范围大于A、C组（P〈0.05）。B组小鼠脑组织及胃黏膜内HSP70的表达均有不同程度的升高,高于A组（P〈0.05）;B、D组脑组织和胃黏膜内细胞凋亡最明显,明显高于A、C组（P〈0.05）;经GGA灌胃后HSP70蛋白表达明显升高,而细胞凋亡指数明显降低,C组的HSP70表达高于B、D组,而细胞凋亡指数低于B、D组（P〈0.05）。结论 GGA灌胃后能够诱导HSP70在脑组织和胃黏膜内的表达;抑制细胞凋亡途径是HSP70保护脑组织和胃黏膜的机制之一;GGA可以用于颅脑创伤急性胃黏膜病变的预防和治疗。 |
| Abstract_FL | Objective To explore the protective mechanism of HSP70 protein in traumatic brain injury (TBI)‐related acute gastric mucosal lesions in mice .Methods Forty adult male Balb/c mice were randomly divided into sham (A) ,TBI (B) ,TBI+ geranylgeranylacetone (GGA) (C) ,and TBI+saline (D) groups .TBI was induced via the Feeney impact model .GGA (800 mg/kg) was administered via oral tube beginning before the model was built in group C .The expressions of HSP70 protein in brain and gastric mucosa were determined by immunohistochemistry , and the apoptotic index was detected by TUNEL method .Results The injury area in mouse brain and gastric mucosa was greater in group B than in groups A and C (P<0 .05) .After model induction ,the content of HSP70 protein in group B was markedly higher in the brain and gastric mucosa ,which was notably higher than in group A (P<0 .05) .Obviously apoptotic cells were observed in groups B and D ,which were significantly higher than in groups A and C .GGA pretreatment enhanced the up‐regulated expression of HSP70 and decreased the apoptotic index distinctly ;HSP70 expression was higher in group C than in groups B and D ,but the apoptotic index was lower (P<0 .05) .Conclusion GGA can induce HSP70 protein expression in mouse brain and gastric mucosa .HSP70 is involved in the process of apoptosis inhibition .GGA can be used in the prevention and therapy of TBI‐related acute gastic mucosal lesions . |
| Author | 严贵忠 王登峰 杨文桢 刘吉星 侯博儒 任海军 |
| AuthorAffiliation | 兰州大学第二医院神经外科,甘肃兰州730030 |
| AuthorAffiliation_xml | – name: 兰州大学第二医院神经外科,甘肃兰州,730030 |
| Author_FL | WANG Deng-feng LIU Ji-xing REN Hai-jun YANG Wen-zhen YAN Gui-zhong HOU Bo-ru |
| Author_FL_xml | – sequence: 1 fullname: YAN Gui-zhong – sequence: 2 fullname: WANG Deng-feng – sequence: 3 fullname: YANG Wen-zhen – sequence: 4 fullname: LIU Ji-xing – sequence: 5 fullname: HOU Bo-ru – sequence: 6 fullname: REN Hai-jun |
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| DOI | 10.7652/jdyxb201604015 |
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| DocumentTitleAlternate | Effects of heat shock protein 70 on mice with traumatic brain injury-related acute gastric mucosal lesions |
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| EndPage | 550 |
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| Keywords | 热休克蛋白70(HSP70) 细胞凋亡 acute gastric mucosal lesions 颅脑创伤 急性胃黏膜病变 heat shock protein 70 traumatic brain injury (TBI) apoptosis |
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| Notes | YAN Gui-zhong, WANG Deng-feng, YANG Wen-zhen, LIU Ji-xing, HOU Bo-ru, REN Hai-jun （Department of Neurosurgery, Lanzhou University Second Hospital, Lanzhou 730030, China） traumatic brain injury （TBI）; acute gastric mucosal lesions; heat shock protein 70; apoptosis Objective To explore the protective mechanism of HSP70 protein in traumatic brain injury （TBI）‐related acute gastric mucosal lesions in mice .Methods Forty adult male Balb/c mice were randomly divided into sham （A） ,TBI （B） ,TBI＋ geranylgeranylacetone （GGA） （C） ,and TBI＋saline （D） groups .TBI was induced via the Feeney impact model .GGA （800 mg/kg） was administered via oral tube beginning before the model was built in group C .The expressions of HSP70 protein in brain and gastric mucosa were determined by immunohistochemistry , and the apoptotic index was detected by TUNEL method .Results The injury area in mouse brain and gastric mucosa was greater in group B than in groups A and C （P〈0 .05） .After model induction ,the content of HSP70 protein in grou |
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| PublicationTitle | 西安交通大学学报（医学版） |
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| Publisher | 兰州大学第二医院神经外科,甘肃兰州,730030 |
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| Snippet | 目的 探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法 40只成年雄性小鼠,随机分为假手术组（A组）、模型组（B组）、模型组＋GGA组（C... R641; 目的：探索热休克蛋白70（HSP70）在小鼠颅脑创伤急性胃黏膜病变模型中的保护作用机制。方法40只成年雄性小鼠，随机分为假手术组（A组）、模型组（B组）、模型组＋ GGA... |
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| SubjectTerms | 急性胃黏膜病变 热休克蛋白70（HSP70） 细胞凋亡 颅脑创伤 |
| Title | 热休克蛋白70对小鼠颅脑创伤相关急性胃黏膜病变的保护作用 |
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