發(fā)布時(shí)間：2018-06-25 07:32

  本文選題：高遷移率族蛋白B1 + 創(chuàng)傷性腦損傷��； 參考：《南京醫(yī)科大學(xué)》2016年博士論文

【摘要】：第一部分急性創(chuàng)傷性腦損傷患者血漿中HMGB1的表達(dá)及臨床意義目的：探討急性創(chuàng)傷性腦損傷患者血漿中高遷移率簇蛋白B1 (High-mobility group box 1,HMGB1)的表達(dá)以及臨床意義。方法：選取2012年1月至2012年6月住院的急性創(chuàng)傷性腦損傷患者142例,輕度腦創(chuàng)傷組68例(GCS 13～15分)；中度腦創(chuàng)傷組48例(GCS 9-12分)；重度腦創(chuàng)傷組26例(GCS 3-8分)。所有患者均于傷后4-6小時(shí)內(nèi)采集上肢靜脈血,并采用酶聯(lián)免疫吸附測定法(Enzyme Linked ImmunoSorbent Assay, ELISA)測定血漿中HMGB1的表達(dá)。并且選取同期體檢健康正常者15例作為對照組。比較腦創(chuàng)傷組和對照組兩者HMGB1的表達(dá)水平,并分析急性創(chuàng)傷性腦損傷患者傷后1個(gè)月內(nèi)死亡和6個(gè)月內(nèi)功能預(yù)后不良的危險(xiǎn)因素。結(jié)果：急性創(chuàng)傷性腦損傷患者血漿中HMGB1水平均比對照組明顯增高(P0.01)；血漿中HMGB1水平與入院時(shí)GCS評分呈顯著負(fù)相關(guān)(P0.01)。單因素Logistic回歸分析顯示,血漿中HMGBl水平是急性創(chuàng)傷性腦損傷患者傷后1個(gè)月內(nèi)死亡和6個(gè)月內(nèi)功能預(yù)后不良的危險(xiǎn)因素。ROC曲線分析顯示血漿中HMGB1水平對急性創(chuàng)傷性腦損傷患者傷后1個(gè)月內(nèi)死亡和6個(gè)月內(nèi)功能預(yù)后不良有顯著預(yù)測價(jià)值。結(jié)論：急性創(chuàng)傷性腦損傷患者血漿中HMGB1表達(dá)水平增高,且其增高的程度與腦傷情的輕重呈正相關(guān),血漿中HMGB1的水平可作為評估腦創(chuàng)傷患者預(yù)后的一項(xiàng)重要觀察指標(biāo)。第二部分HMGB1在實(shí)驗(yàn)性大鼠急性創(chuàng)傷性腦損傷中的表達(dá)目的：探討實(shí)驗(yàn)性大鼠急性創(chuàng)傷性腦損傷后HMGB1在血漿和腦組織中的表達(dá)情況,以及腦水腫和細(xì)胞凋亡情況。方法：大鼠隨機(jī)分為7組：假手術(shù)組、腦創(chuàng)傷2h組、腦創(chuàng)傷6h組、腦創(chuàng)傷12h組、腦創(chuàng)傷24h組、腦創(chuàng)傷48h組、腦創(chuàng)傷72h組(每組12只),改良Feeney重物自由落體法建立大鼠腦創(chuàng)傷模型,ELISA檢測血漿中HMGB1的表達(dá),免疫組化染色觀察HMGB1陽性細(xì)胞的表達(dá),濕/干法測定腦水含量,TUNEL染色檢測細(xì)胞凋亡。結(jié)果：血漿中HMGB1在假手術(shù)組為0.83±0.15ng/ml,傷后2h為3.50±0.57ng/m1(與假手術(shù)組相比P0.01),傷后6h為7.87±0.60ng/ml(與傷后2h相比尸0.01),傷后12h為7.85±0.59ng/ml,傷后24h為7.6l±0.66ng/ml(腦創(chuàng)傷6h組、腦創(chuàng)傷12h組、腦創(chuàng)傷24h組各組間相比尸0.05),傷后48h為4.63±0.68ng/ml(與傷后24h相比P0.01),傷后72h為3.11±0.66ng/ml(與傷后48h相比P0.01);HMGB1陽性細(xì)胞在假手術(shù)組為7.49±1.76%,傷后2h為36.54±5.92%(與假手術(shù)組相比P0.01),傷后6h為65.58±5.46%(與傷后2h相比尸0.01),傷后12h為65.18±4.83%,傷后24h為64.68±4.09%(腦創(chuàng)傷6h組、腦創(chuàng)傷12h組、腦創(chuàng)傷24h組各組間相比P0.05),傷后48h為43.17±4.48%(與傷后24h相比P0.01),傷后72h為36.50±4.92%(與傷后48h相比P0.01)；傷側(cè)腦組織含水量在假手術(shù)組為79.21±0.96%,傷后2h為79.27±0.92%(與假手術(shù)組相比尸0.05),傷后6h為81.00±0.85%(與傷后2h組相比P0.01),傷后12h為82.26±0.95%(與傷后6h組相比P0.05),傷后24h為83.54±0.93%(與傷后12h組相比P0.05),傷后48h為82.31±0.50%(與傷后24h組相比P0.05),傷后72h為81.22±0.88%(與傷后48h組相比P0.05)；細(xì)胞凋亡在假手術(shù)組為6.62±1.38%,傷后2h為8.73±1.52%(與假手術(shù)組相比P0.05),傷后6h為35.11±4.72%(與傷后2h組相比P0.01),傷后12h為43.23±4.61%(與傷后6h組相比P0.05),傷后24h為52.29±4.76%(與腦創(chuàng)傷12h組相比尸0.01),傷后48h為39.91±4.66%(與腦創(chuàng)傷24h組相比P0.01),傷后72h為32.56±4.85%(與腦創(chuàng)傷48h組相比P0.05)。結(jié)論：大鼠腦創(chuàng)傷后血漿中HMGB1在傷后2h開始升高,傷后6h達(dá)到峰值,持續(xù)24h,傷后48h開始明顯下降；大鼠腦創(chuàng)傷后2h HMGB1由細(xì)胞核向細(xì)胞質(zhì)分布,傷后6h達(dá)到峰值,持續(xù)24h,傷后48h開始明顯下降；大鼠腦創(chuàng)傷后6h傷側(cè)腦組織含水量開始升高,至傷后24h達(dá)高峰,傷后48h開始有所緩解；大鼠腦創(chuàng)傷后傷后6h凋亡細(xì)胞逐步增多,傷后24h達(dá)到最多,傷后48h逐步減少。第三部分甘草酸苷對大鼠腦創(chuàng)傷后HMGB1表達(dá)的影響及其作用機(jī)制探討目的：探討甘草酸苷對大鼠創(chuàng)傷性腦損傷的神經(jīng)保護(hù)作用和對高遷移率族蛋白B1 (HMGB1)的影響。方法：雄性SD大鼠隨機(jī)分為三組：假手術(shù)組、腦創(chuàng)傷組、甘草酸苷組(每組36只)。采用改良Feeney法建立大鼠腦創(chuàng)傷模型。在甘草酸苷組,傷后30分鐘靜脈注射10mg/kg甘草酸苷。傷后24小時(shí)行運(yùn)動功能、腦組織含水量測定,同時(shí)在損傷部位周圍的腦組織采樣,用RT-PCR、Western blot、 EMSA和ELISA方法檢測HMGB1/HMGB1的受體(TLR4和RAGE)/NF-κB的信號通路和炎性細(xì)胞因子,并且分析HMGB1、RAGE和TLR4免疫組化和細(xì)胞凋亡的情況。結(jié)果：腦創(chuàng)傷組明顯引起運(yùn)動功能障礙(與假手術(shù)組相比P0.01),甘草酸苷組運(yùn)動功能受損明顯減輕(與腦創(chuàng)傷組比較,P0.01)；損傷側(cè)腦組織含水量在假手術(shù)組為79.97±0.82%,在腦創(chuàng)傷組為82.94±0.65%(與假手術(shù)組相比,P0.01),在甘草酸苷組為80.97±0.49%(與腦創(chuàng)傷組相比,P0.01)；創(chuàng)傷性腦損傷區(qū)周圍腦組織HMGB1/HMGB1受體(TLR.4和RAGE) /NF-κB信號通路表達(dá)顯著增加(與假手術(shù)組相比,各指標(biāo)P0.01)。甘草酸苷治療后,HMGB1/HMGB1受體(TLR.4和RAGE)/NF-κB信號通路表達(dá)受到抑制(與腦創(chuàng)傷組相比,各指標(biāo)P0.05)；假手術(shù)組大鼠腦組織IL-1β、TNF-α和IL-6的含量分別為39.48±5.67pg/mg、10.52±1.53pg/mg、5.38±0.82pg/mg,腦創(chuàng)傷組大鼠腦組織IL-1β、TNF-α和IL-6的含量分別為79.57±5.17pg/mg、 18.94±1.45pg/mg、16.08±1.06pg/mg(與假手術(shù)組相比,各指標(biāo)P0.01),甘草酸苷組大鼠腦組織IL-1β、TNF-α和IL-6的含量為62.02±5.54pg/mg、15.25 ±1.52pg/mg、11.60±0.90pg/mg(與腦創(chuàng)傷組相比,各指標(biāo)P0.01)；.在假手術(shù)組HMGB1、RAGE和TLR4陽性細(xì)胞及凋亡細(xì)胞分別為7.98±1.44%、5.60±1.12%、7.60±1.29%、8.19±1.46%,在腦創(chuàng)傷組HMGB1、RAGE和TLR4陽性細(xì)胞及凋亡細(xì)胞分別為58.37±5.06%、54.15±4.65%、65.50±4.83%、52.02±4.63%(與假手術(shù)組相比,各指標(biāo)P0.01),在甘草酸苷組分別為39.99±4.99%,34.87±5.02%,43.33±4.54%,37.84±5.16%(與腦創(chuàng)傷組相比,各指標(biāo)P0.01)。結(jié)論：甘草酸苷下調(diào)大鼠創(chuàng)傷周圍腦組織HMGB1/HMGB1受體(TLR4和RAGE)/NF-κB介導(dǎo)的炎癥反應(yīng),減輕繼發(fā)性腦損傷,改善大鼠腦創(chuàng)傷的預(yù)后。我們的研究表明甘草酸苷對大鼠創(chuàng)傷性腦損傷具有神經(jīng)保護(hù)作用。
[Abstract]:The expression and clinical significance of HMGB1 in the first part of the patients with acute traumatic brain injury: To explore the expression and clinical significance of high mobility cluster protein B1 (High-mobility group box 1, HMGB1) in patients with acute traumatic brain injury and its clinical significance. Methods: 1 patients with acute traumatic brain injury from January 2012 to June 2012 were selected. 42 cases, 68 cases of mild brain trauma (GCS 13~15), 48 cases of moderate brain trauma (GCS 9-12) and 26 cases of severe brain trauma (GCS 3-8). All patients collected upper limb venous blood within 4-6 hours after injury, and the expression of HMGB1 in plasma was determined by enzyme linked immunosorbent assay (Enzyme Linked ImmunoSorbent Assay, ELISA). 15 cases of healthy and normal physical examination were taken as control group. The expression level of HMGB1 in both brain trauma group and control group was compared, and the risk factors of poor functional prognosis within 1 months after acute traumatic brain injury and 6 months after injury were analyzed. Results: the plasma levels of HMGB1 in patients with acute traumatic brain injury were significantly higher than those in the control group. High (P0.01); HMGB1 level in plasma was negatively correlated with GCS score at admission (P0.01). Single factor Logistic regression analysis showed that HMGBl level in plasma was a risk factor for acute traumatic brain injury within 1 months of injury and a risk factor for poor functional prognosis within 1 months of injury, and.ROC curve analysis showed that the level of HMGB1 in plasma was acute to acute traumatic injury. Conclusion: the level of HMGB1 expression in the plasma of patients with acute traumatic brain injury is higher, and the degree of the increase is positively correlated with the severity of brain injury. The level of HMGB1 in plasma can be an important observation to evaluate the prognosis of patients with brain injury. Index. Second part HMGB1 expression in experimental rat acute traumatic brain injury. Objective: To investigate the expression of HMGB1 in plasma and brain tissue after acute traumatic brain injury in experimental rats, as well as brain edema and apoptosis. Methods: rats were randomly divided into 7 groups: sham operation group, brain trauma 2H group, brain trauma 6h group, brain Group 12h, group 24h of brain trauma, group 48h of brain trauma, group of brain trauma, group 72h (each group of 12), modified Feeney weight free falling body method to establish rat brain trauma model, ELISA to detect the expression of HMGB1 in plasma, immunohistochemical staining to observe the expression of HMGB1 positive cells, wet / dry assay of brain water content, TUNEL staining to detect cell apoptosis. Results: H in the plasma. MGB1 was 0.83 + 0.15ng/ml in the sham operation group and 3.50 + 0.57ng/m1 after injury (compared with that of the sham group) (compared with the sham operation group), and the 6h was 7.87 + 0.60ng/ml (0.01) after injury (compared with 2h after injury), and the 12h was 7.85 + 0.59ng/ml after injury. The 24h was 7.6l + 0.05 after injury (group of brain trauma, brain trauma group, 0.05 of all groups of brain trauma groups), and 4.63 + 0.05 after injury. (compared with 24h after injury P0.01), 72h was 3.11 + 0.66ng/ml after injury (compared with 48h after injury); HMGB1 positive cells were 7.49 + 1.76% in sham operation group and 36.54 + 5.92% after injury (P0.01 compared to sham operation group), 6h was 65.58 + 5.46% after injury (0.01), 65.18 + 4.83% after injury, and after injury, it was 64.68 + 4.09% (brain trauma group, brain creation) 12h group was injured in group 12h and group 24h was compared with P0.05 in group 24h (compared with 24h P0.01 after injury), and 72h was 36.50 + 4.92% (P0.01 compared with 48h after injury). The water content of the injured brain tissue was 79.21 + 0.96% in sham operation group and 79.27 + 0.92% after injury (0.05 in sham operation group) and 81 + 0.85% after injury. 12h was 82.26 + (P0.05) after injury (compared with group 6h after injury), 24h was 83.54 + 0.93% (P0.05 compared with group 12h) and 48h was 82.31 + 0.50% (compared with group 24h after injury), and 81.22 + 0.88% (compared with 48h group after injury); apoptosis was 6.62 + 1.38% in sham operation group and 8.73 + 1.52% (and artificial hand) after injury. Compared with P0.05, 6h was 35.11 + 4.72% (P0.01 compared with group 2H), 12h was 43.23 + 4.61% (P0.05 compared with group 6h), 24h was 52.29 + 4.76% after injury (0.01), and 48h was 39.91 + 4.66% (compared to 24h group of brain trauma) after injury, and 32.56 + (compared with brain trauma group). After traumatic brain injury, the plasma HMGB1 began to rise in 2h after injury, and the 6h reached its peak after injury. After the injury, the 48h began to decrease obviously after injury. After the injury, the 2H HMGB1 was distributed to the cytoplasm of the nucleus to the cytoplasm, and the 6h reached the peak after injury. The 48h began to decrease obviously after injury, and the water content in the 6h injured brain tissue began to rise after the traumatic brain injury. After injury, 24h reached a peak, and 48h began to remission after injury; 6h apoptotic cells gradually increased after traumatic brain injury in rats, the 24h reached most after injury, and 48h gradually decreased after injury. The effect and mechanism of third part of glycyrrhizin on HMGB1 expression after traumatic brain injury in rats and its mechanism of action were discussed. Methods: the effect of protective action and high mobility group protein B1 (HMGB1). Methods: male SD rats were randomly divided into three groups: sham operation group, brain trauma group and glycyrrhizin group (36 rats in each group). The rat model of brain trauma was established by improved Feeney method. In the glycyrrhizin group, 10mg/kg glycyrrhizin was injected into the vein 30 minutes after injury. The exercise function was performed after 24 hours after injury. The water content of brain tissue was measured, and the brain tissue around the injured part was sampled. RT-PCR, Western blot, EMSA and ELISA methods were used to detect the signaling pathway and inflammatory cytokines of HMGB1/HMGB1 receptor (TLR4 and RAGE) /NF- kappa B, and HMGB1, RAGE and immunohistochemical and apoptosis were analyzed. The motor dysfunction in the glycyrrhizin group was significantly reduced (compared with the brain trauma group, P0.01), and the water content of the injured side brain tissue was 79.97 + 0.82% in the sham operation group and 82.94 + 0.65% in the brain trauma group (compared with the sham group, P0.01) and 80.97 + 0.49% in the glycyrrhizin group (compared with the brain trauma group, P0.0, compared with the brain trauma group, P0.0). 1): the expression of HMGB1/HMGB1 receptor (TLR.4 and RAGE) /NF- kappa B signaling pathway in the peripheral brain tissue of the traumatic brain injury area was significantly increased (compared with the sham operation group, P0.01). After glycyrrhizin treatment, the expression of HMGB1/HMGB1 receptor (TLR.4 and RAGE) /NF- kappa B signaling pathway was suppressed (compared with the brain trauma group, each index P0.05); sham operation group rats. The content of IL-1 beta, TNF- alpha and IL-6 in brain tissue was 39.48 + 5.67pg/mg, 10.52 + 1.53pg/mg and 5.38 + 0.82pg/mg respectively. The content of IL-1 beta, TNF- A and IL-6 in brain tissue of brain trauma rats were 79.57 + 5.17pg/mg, 18.94 + 1.45pg/mg, 16.08 + 1.06pg/mg (compared with sham operation group). The content of L-6 was 62.02 + 5.54pg/mg, 15.25 + 1.52pg/mg and 11.60 + 0.90pg/mg (P0.01), respectively. In the sham operation group HMGB1, RAGE and TLR4 positive cells and apoptotic cells were 7.98 + 1.44%, 5.60 + 1.12%, 7.60 + 1.29% and 8.19 +, respectively, in the brain trauma group, and RAGE and TLR4 positive cells and apoptotic cells were 58.37. 5.06%, 54.15 + 4.65%, 65.50 + 4.83%, 52.02 + 4.63% (compared with the sham operation group, each index P0.01), in the glycyrrhizin group were 39.99 + 4.99%, 34.87 + 5.02%, 43.33 + 4.54%, 37.84 +, respectively (compared with the brain trauma group, each index P0.01). Conclusion: glycyrrhizin downregulated the HMGB1/HMGB1 receptor (TLR4 and RAGE) of /NF- kappa B in the brain tissue around the trauma of rats The inflammatory response alleviates secondary brain damage and improves the prognosis of brain trauma in rats. Our study shows that glycyrrhizin has a neuroprotective effect on traumatic brain injury in rats.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R651.15

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