抑郁症的病理机制复杂,研究表明神经炎症在抑郁症的病理机制中发挥着重要作用。高迁移率族蛋白1(high mobility group box 1,HMGB1)是一种广泛存在于哺乳动物真核细胞内的非组蛋白DNA结合蛋白,释放至胞外后可引发炎症性级联反应,继而导...抑郁症的病理机制复杂,研究表明神经炎症在抑郁症的病理机制中发挥着重要作用。高迁移率族蛋白1(high mobility group box 1,HMGB1)是一种广泛存在于哺乳动物真核细胞内的非组蛋白DNA结合蛋白,释放至胞外后可引发炎症性级联反应,继而导致抑郁症的发生。本文对HMGB1在抑郁症中可能涉及的病理机制进行综述,以期为后续研究提供借鉴。展开更多
目的观察不同剂量他汀类药物治疗对动脉粥样硬化性脑梗死患者血浆S100B和高迁移率族蛋白B1(highmobility group protein B1,HMGB1)水平的影响。方法选择大动脉粥样硬化性脑梗死患者298例,根据服用阿托伐他汀钙剂量分为他汀高剂量(40mg/...目的观察不同剂量他汀类药物治疗对动脉粥样硬化性脑梗死患者血浆S100B和高迁移率族蛋白B1(highmobility group protein B1,HMGB1)水平的影响。方法选择大动脉粥样硬化性脑梗死患者298例,根据服用阿托伐他汀钙剂量分为他汀高剂量(40mg/晚)组106例,他汀标准剂量(20mg/晚)组134例,他汀空白组58例,另选择健康体检者67例作为对照组。记录各组入院时、7d血浆S100B、HMGB1水平及美国国立卫生研究院卒中量表(NIHSS)评分。结果他汀高剂量组、他汀标准剂量组、他汀空白组入院时S100B水平较对照组明显升高[(38.19±30.10)pg/L,(38.41±23.75)pg/L,(32.47±25.04)pg/L vs(24.57±12.15)pg/L,P<0.05,P<0.01]。与他汀空白组比较,他汀高剂量组、他汀标准剂量组7d时S100B水平明显降低(P<0.05)。与他汀标准剂量组比较,他汀高剂量组7d时S100B水平明显降低(P<0.05)。与入院时比较,他汀空白组7d时S100B水平明显升高,他汀高剂量组7d时S100B水平明显降低(P<0.05,P<0.01)。入院时S100B水平与HDL-C(r=-0.224,P=0.010)、脑梗死体积(r=0.272,P=0.004)相关。结论阿托伐他汀钙不仅能调节血脂水平,还能降低炎性因子S100B水平,可能是其发挥抗炎及神经保护功能的机制之一。展开更多
High-mobility-group B1 (HMGB1), an abundant, highly conserved cellular protein, is widely known as a nuclear DNA-binding protein that stabilizes nucleosome formation, and facilitates gene transcription. Recent studies...High-mobility-group B1 (HMGB1), an abundant, highly conserved cellular protein, is widely known as a nuclear DNA-binding protein that stabilizes nucleosome formation, and facilitates gene transcription. Recent studies suggested that HMGB1 could be overexpressed and released from cellular nucleosome upon endotoxin and cytokine stimulation, or other stress challenge including burns, shock, as well as infection. Therefore, extracellular HMGB1 might be involved in the pathogenesis of sepsis and subsequent multiple organ dysfunction syndrome. Moreover, experimental data showed that extracellular HMGB1 might play vital roles in nerves development, tumor metastasis, atherosclerosis and restenosis after vascular damage.展开更多
High mobility group box-1(HMGB1)distributed widely.It exists in many organs.HMGB1 locates in nuclei and cytoplasm in normal condition.It involves in many activity of life(i.e.,duplication of DNA,cellular differentiati...High mobility group box-1(HMGB1)distributed widely.It exists in many organs.HMGB1 locates in nuclei and cytoplasm in normal condition.It involves in many activity of life(i.e.,duplication of DNA,cellular differentiation,gene expression).The immunocytes(i.e.,mononuclear macrophage and dendritic cells)secrete HMGB1 into the extracellular milieu when stimulated with LPS and cytokines.It acts as proinflammatory cytokines,activates inflammatory and immunological responses.As a late mediators of inflammation and last long,HMGB1 plays an important role in sepsis,so it may be a convenient and practical index in evaluating severity of sepsis and may be an important and new therapeutic target in sepsis.It has been initially proved in experimental and clinical study.展开更多
目的研究急性脑梗死患者血清高迁移率族蛋白B1(HMGBl)与外周血淋巴细胞过氧化小体增殖剂激活型受体γ(PPARγ)mRNA表达的变化,及二者与脑梗死体积的相关性。方法连续收集2010年7月—12月哈尔滨医科大学附属第二医院老年病科及神经内科...目的研究急性脑梗死患者血清高迁移率族蛋白B1(HMGBl)与外周血淋巴细胞过氧化小体增殖剂激活型受体γ(PPARγ)mRNA表达的变化,及二者与脑梗死体积的相关性。方法连续收集2010年7月—12月哈尔滨医科大学附属第二医院老年病科及神经内科就诊的发病3 d以内的急性脑梗死患者72例及对照人群70例。用ELISA法测定两组患者血清中HMGB1,用实时RT-PCR法测定两组患者空腹周围血淋巴细胞PPARγmRNA的表达情况。根据脑梗死患者发病后48～72 h CT检查结果,计算脑梗死体积。结果①梗死组患者PPA脚mRNA表达水平(0.54±0.37)低于对照组(1.98±0.35),血清HMGBl水平(12.7±6.1)μg/L高于对照组(2.2±0.8)μg/L,差异有统计学意义,P<0.01。②脑梗死患者周围血淋巴细胞PPA脚mRNA表达水平与血清HMGBl水平呈负相关,r=-0.843,P<0.01。③经相关性分析,脑梗死患者PPARγmRNA表达水平与脑梗死体积呈负相关,r=-0.886,P<0.01;脑梗死患者HMGB1水平和脑梗死体积呈正相关,r=0.847,P<0.01。结论在脑梗死急性期,PPARγ和HMGB1均参与脑缺血炎性反应,HMGB1及PPARγ脚mRNA表达水平可反映急性脑梗死患者梗死体积的大小。展开更多
文摘抑郁症的病理机制复杂,研究表明神经炎症在抑郁症的病理机制中发挥着重要作用。高迁移率族蛋白1(high mobility group box 1,HMGB1)是一种广泛存在于哺乳动物真核细胞内的非组蛋白DNA结合蛋白,释放至胞外后可引发炎症性级联反应,继而导致抑郁症的发生。本文对HMGB1在抑郁症中可能涉及的病理机制进行综述,以期为后续研究提供借鉴。
文摘目的观察不同剂量他汀类药物治疗对动脉粥样硬化性脑梗死患者血浆S100B和高迁移率族蛋白B1(highmobility group protein B1,HMGB1)水平的影响。方法选择大动脉粥样硬化性脑梗死患者298例,根据服用阿托伐他汀钙剂量分为他汀高剂量(40mg/晚)组106例,他汀标准剂量(20mg/晚)组134例,他汀空白组58例,另选择健康体检者67例作为对照组。记录各组入院时、7d血浆S100B、HMGB1水平及美国国立卫生研究院卒中量表(NIHSS)评分。结果他汀高剂量组、他汀标准剂量组、他汀空白组入院时S100B水平较对照组明显升高[(38.19±30.10)pg/L,(38.41±23.75)pg/L,(32.47±25.04)pg/L vs(24.57±12.15)pg/L,P<0.05,P<0.01]。与他汀空白组比较,他汀高剂量组、他汀标准剂量组7d时S100B水平明显降低(P<0.05)。与他汀标准剂量组比较,他汀高剂量组7d时S100B水平明显降低(P<0.05)。与入院时比较,他汀空白组7d时S100B水平明显升高,他汀高剂量组7d时S100B水平明显降低(P<0.05,P<0.01)。入院时S100B水平与HDL-C(r=-0.224,P=0.010)、脑梗死体积(r=0.272,P=0.004)相关。结论阿托伐他汀钙不仅能调节血脂水平,还能降低炎性因子S100B水平,可能是其发挥抗炎及神经保护功能的机制之一。
文摘High-mobility-group B1 (HMGB1), an abundant, highly conserved cellular protein, is widely known as a nuclear DNA-binding protein that stabilizes nucleosome formation, and facilitates gene transcription. Recent studies suggested that HMGB1 could be overexpressed and released from cellular nucleosome upon endotoxin and cytokine stimulation, or other stress challenge including burns, shock, as well as infection. Therefore, extracellular HMGB1 might be involved in the pathogenesis of sepsis and subsequent multiple organ dysfunction syndrome. Moreover, experimental data showed that extracellular HMGB1 might play vital roles in nerves development, tumor metastasis, atherosclerosis and restenosis after vascular damage.
文摘High mobility group box-1(HMGB1)distributed widely.It exists in many organs.HMGB1 locates in nuclei and cytoplasm in normal condition.It involves in many activity of life(i.e.,duplication of DNA,cellular differentiation,gene expression).The immunocytes(i.e.,mononuclear macrophage and dendritic cells)secrete HMGB1 into the extracellular milieu when stimulated with LPS and cytokines.It acts as proinflammatory cytokines,activates inflammatory and immunological responses.As a late mediators of inflammation and last long,HMGB1 plays an important role in sepsis,so it may be a convenient and practical index in evaluating severity of sepsis and may be an important and new therapeutic target in sepsis.It has been initially proved in experimental and clinical study.
文摘目的研究急性脑梗死患者血清高迁移率族蛋白B1(HMGBl)与外周血淋巴细胞过氧化小体增殖剂激活型受体γ(PPARγ)mRNA表达的变化,及二者与脑梗死体积的相关性。方法连续收集2010年7月—12月哈尔滨医科大学附属第二医院老年病科及神经内科就诊的发病3 d以内的急性脑梗死患者72例及对照人群70例。用ELISA法测定两组患者血清中HMGB1,用实时RT-PCR法测定两组患者空腹周围血淋巴细胞PPARγmRNA的表达情况。根据脑梗死患者发病后48～72 h CT检查结果,计算脑梗死体积。结果①梗死组患者PPA脚mRNA表达水平(0.54±0.37)低于对照组(1.98±0.35),血清HMGBl水平(12.7±6.1)μg/L高于对照组(2.2±0.8)μg/L,差异有统计学意义,P<0.01。②脑梗死患者周围血淋巴细胞PPA脚mRNA表达水平与血清HMGBl水平呈负相关,r=-0.843,P<0.01。③经相关性分析,脑梗死患者PPARγmRNA表达水平与脑梗死体积呈负相关,r=-0.886,P<0.01;脑梗死患者HMGB1水平和脑梗死体积呈正相关,r=0.847,P<0.01。结论在脑梗死急性期,PPARγ和HMGB1均参与脑缺血炎性反应,HMGB1及PPARγ脚mRNA表达水平可反映急性脑梗死患者梗死体积的大小。
