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Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.  相似文献   

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Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.  相似文献   

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Objective To evaluate the effect of artemether on the cell cycle and the radiosensitivity in human nasopharyngeal carcinoma cell line CNE-1.Methods Cell growth inhibition was assessed with MTT.The method of colony-forming was used to detect the radiation sensitivity.Cell cycle distribution was analyzed by using flow cytometry.The protein expressions of clyclin B1 and Weei were detected by using Western blot.Results The growth of CNE-1 cells was inhibited in a dose-dependent manner.The concentration of 20 μmol/L artemether had radiosensitive effect on CNE-1 cells at 24 h after administration,and SER was 1.481.When CNE-1 cell was irradiated,the G2/M cells increased (t =4.59,P < 0.05).After exposure to combination of artemether and irradiation,the G2/M cells were decreased (t= 10.60,P < 0.05).Western blot showed that artemether increased the level of cyclin B1 expression and inhibited the level of Weel expression.Conclusions The noncytotoxic concentration of artemether could enhance radiosensitization of CNE-1 cells.The radiosensitivity enhancement of artemether might depend on the exposure time.The effect is most obvious when radiation is delivered 24 h after expose to artemetherr.The radiosensitizing effect could be related to apoptosis.  相似文献   

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Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.  相似文献   

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Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.  相似文献   

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Objective To investigate effects of different rewarming rates and maintenance of light hypothermia on inflammatory response in rabbits after limb blast injury, coupled with seawater immersion. Methods First, the model of limb blast injury coupled with seawater immersion was reproduced [the animals were immersed to low body temperature of (31.0±0.5℃)]. Then, 24 adult rabbits were randomly divided into group Ⅰ [the rapid rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (8.94±0.93)℃/h], group Ⅱ [the slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (3.88±0.22)℃/h], group Ⅲ [another slow rewarming group, n=6, rewarmed to (38±0.5)℃ at a rate of (2.18±0.12)℃/h], and the H group [the hypothermia group, n =6, rewarmed to (34 - 35)℃ at a rate of (4.49±0.66)℃/h and kept at that temperature till termination of the experiment]. Regulation of ambient temperature and warm transfusion were used to restore body temperature to target levels and maintained there for 6 hours. Blood samples were taken at 5 different times, I.e. Pre-injury time(T0), post-immersion time (T1), the time when rewarming started (T2), 3 h after rewarming (T3), and 6 h after rewarming (T4). Tissue samples from heart, liver, intestinum, lung and kidney were also collected. Levels of TNF-α (tumor necrosis factor-α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in plasma and MPO (myeloperoxidase) in homogenate were detected. Results Following rewarming, TNF-α, IL-1β, IL-6 concentrations in the plasma of the animals in group Ⅰ and group H were significantly higher when compared with those of the animals in group Ⅱ and group Ⅲ (P<0.05, P<0.01), and MPO activity in homogenate was significantly higher when compared with that of the animals in group Ⅱ and group Ⅲ(P<0.01, P<0.05), and no statistical difference could be seen between group Ⅱ and Ⅲ (P>0.05). Conclusions Rapid rewarming and maintenance of light hypothermia could obviously elevate TNF-α, IL-1β, IL-6 concentrations in plasma and MPO activity in homogenate, following limb blast injury coupled with hypothermia induced by seawater immersion, while slow rewarming (with a rewarming rate of 2-4℃/h) could significantly inhibit TNF-α, IL-1β, IL-6 levels and PMN activity.  相似文献   

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目的 探讨新型氧自由基清除剂依达拉奉对中、重型颅脑外伤患者血清神经元特异性烯醇化酶(neuron-specific enolase,NSE)和S100β蛋白浓度的影响.方法 选取中、重型颅脑外伤手术患者90例,将患者分为对照组(A组)、手术后应用依达拉奉组(B组)和手术前应用依达拉奉组(C组),各组30例,同时取门诊健康体检者20例作为健康对照组.采用ELISA法测定各组入院时以及手术后1,3,5,7 d外周静脉血血清NSE和S100β浓度.结果 A组、B组租C组患者血清NSE和S100β蛋白浓度在入院时及手术后1,3,5,7 d明显高于健康对照组,并在手术后第1天达高峰(P<0.05).术后第1天,C组与对照组、A组、B组比较,血清NSE和S100β蛋白浓度降低(P<0.05);A组与B组之间差异无统计学意义(P>0.05).术后第3,5,7天,C组与A组比较,血清NSE和S100β蛋白浓度降低(P<0.05);C组与B组比较,重型患者血清NSE和S100β蛋白浓度降低(P<0.05),但中型患者血清NSE和S100β蛋白浓度差异无统计学意义(P>0.05);B组与A组比较,血清NSE和S100β蛋白浓度降低(P<0.05).结论 依达拉奉能有效降低中、重型颅脑外伤手术患者血清NSE和S100β蛋白浓度,越早使用降低越明显,特别是对于重型颅脑外伤手术患者,手术前应用依达拉奉能更有效地降低血清NSE和S100β蛋白浓度.
Abstract:
Objective To evaluate the effect of edaravone on moderate and severe brain injury patients by observing the change of the serum neuron-specific enolase ( NSE) and S100β protein. Methods A total of 90 patients with acute moderate and severe brain injury were selected and randomly divided into three groups, ie, control group (Group A), postoperative edaravone treatment group (Group B) and preoperative edaravone treatment group (Group C), 30 patients per group. In the meantime, 20 normal persons were set as the healthy control group. The concentrations of serum NSE and S100β protein of each group was measured by using the enzyme-linked immunosorbent assay ( ELISA) on admission and at days 1,3,5 and 7 after operation. Results The serum NSE and S100β protein levels in the Group A, B and C was higher than that in the healthy group on admission and at days 1,3,5 and 7 postoperatively and reached the peak at day 1 after operation (P <0.05). The level of serum NSE and S100β protein in the Group C was lower than that in the healthy group, Group A and Group B at day 1 postoperatively (P<0.05), with no statistical difference between Group B and Group A at day 1 postoperatively (P >0.05). The serum NSE and S100β protein levels in the Group C was lower than that in the Group A at days 3, 5 and 7 postoperatively (P <0.05). The serum NSE and S100β protein levels in the Group C with severe brain injury was lower than that in the Group B at days 3, 5 and 7 postoperatively (P < 0.05), but there was no statistical difference in moderate injury group between Croup C and Group B. The serum NSE and S100β levels in the Group B was lower than that in the Group A at days 3, 5 and 7 postoperatively ( P < 0. 05). Conclusions Edaravone can effectively reduce the serum NSE and S100β levels in the moderate and severe brain injury patients after operation. The earlier use of edaravone may beget the more significant effect, especially in patients with severe brain injury. The application of edaravone before operation can more effectively reduce the concentration of serum NSE and S100β protein.  相似文献   

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目的 研究静脉移植骨髓间充质干细胞(bone martow stromal cells,BMSCs)对大鼠脊髓损伤后功能恢复的影响.方法 对10只同种异体SD大鼠的BMSCs进行体外分离、培养、扩增、纯化后用5-溴脱氧尿嘧啶核苷(5-bromodeoxyuridine,BrdU)进行标记;重物打击致瘫痪造模法制成完全性截瘫的同种大鼠脊髓损伤动物模型,制模后7 d完全随机分为A、B、C三组:A组22只,作为BMSCs移植组,经鼠尾静脉注射2×106/ml的BMSCs细胞悬液1 ml;B组22只,作为对照组,注射1 ml培养液;C组22只,作为空白手术对照组.注射后2,3,6周,免疫组织化学检测BMSCs在损伤段脊髓的存活、分布、分化并计数,观察损伤段脊髓内生长相关蛋白-43(growth associated protein-43,GAP-43)、神经丝蛋白200(neurofilament 200,NF200)和巢蛋白的表达,注射后1,2,3,4,5,6周Basso-Beattie-Bresnaban(BBB)评分评估各组后肢运动功能.结果 移植后2,3,6周BrdU阳性的BMSCs主要分布于损伤段及邻近节段脊髓内.计数发现,移植后2周BrdU阳性的BMSCs约占移植细胞数的4.9%,3周占4.4%,6周占2.9%;移植后2周,BMSCs形态大多变为圆形或椭圆形,部分阳性标记的细胞长出神经元样突起,约12.6%表达胶质纤维酸性蛋白(glial fribrillary acidic protein,GAFP),约5.4%表达神经元特异性核蛋白(neuronal nuclear antigen,NeuN);移植后2,3,6周,A组GAP-43、NF200、巢蛋白的表达明显高于B、C组(P<0.05);移植后3周开始,A组的BBB评分在各观察时相点明显高于B、C组(P<0.05).结论 通过静脉注射的BMSCs能向脊髓损伤灶内迁徙、存活,表现出对损伤灶的趋化性,并向神经元和星形胶质细胞分化,上调GAP-43、NF200和巢蛋白的表达,改善神经功能,可用于脊髓损伤的细胞移植治疗.  相似文献   

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目的探讨亚低温治疗重型颅脑损伤患者临床疗效及对患者血清神经胶质纤维酸性蛋白(GFAP)、泛素羧基末端水解酶L1(UCH-L1)、神经元特异性烯醇化酶(NSE)、C反应蛋白(CRP)水平的影响。方法 106例重型颅脑损伤患者根据随机数字表法分为治疗组(n=53)和对照组(n=53)。对照组给予降低颅内压、脱水以及营养脑细胞等常规治疗,治疗组在对照组基础上结合亚低温治疗。对比分析两组入院时、治疗后1d和治疗后5d颅内压、血糖、血清GFAP、UCH-L1、NSE、CRP指标变化以及治疗6个月后预后情况。结果两组颅内压第1天、第5天较入院时明显降低(P0.05);治疗组治疗后1、5d颅内压明显低于对照组(P0.05);两组第1、第5天血糖水平显著低于入院时(P0.05);治疗组治疗后1、5d血糖水平显著低于同期对照组(P0.05);两组血清GFAP、UCH-L1水平治疗后1、5d较入院时显著降低(P0.05);治疗组血清GFAP、UCH-L1水平治疗后1、5d显著低于对照组(P0.05);两组NSE、CRP水平治疗前比较差异无统计学意义(P0.05);治疗组NSE、CRP治疗后1d和5d明显低于同期对照组(P0.05);治疗组良好率显著高于对照组(P0.05),病死率显著低于对照组(P0.05);而两组中残、重残及植物状态对比差异无统计学意义(P0.05)。结论亚低温治疗重型颅脑损伤患者临床疗效显著,降低血清GFAP、UCH-L1、NSE、CRP水平,改善患者预后,值得进一步推广应用。  相似文献   

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目的 探讨不同程度创伤性脑损伤(traumatic brain injury,TBI)对伤后胚胎神经干细胞(neural stem cells,NSCs)移植的影响. 方法 从孕12~ 14 d胚胎大鼠海马组织中分离NSCs,采用无血清培养法,进行体外培养、扩增和鉴定.大鼠分别于轻型、中型TBI后3d行胚胎NSCs双侧海马区移植;细胞移植14 d后行组织学和TUNEL检测,并对BrdU、NSE、GFAP、GalC、NGF、BDNF蛋白行免疫组化检测. 结果 移植治疗后14 d,轻型TBI组双侧海马区Brdu阳性细胞数明显多于中型TBI组.移植胚胎NSCs脑内分化以GFAP阳性胶质细胞为主.轻、中型TBI后NGF和BDNF蛋白阳性表达增加,其中以轻型TBI组表达最为显著. 结论 轻型和中型TBI对NSCs移植的影响与伤后脑组织局部微环境因素的改变密切相关.  相似文献   

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创伤性脑损伤亚低温治疗期间实施干细胞移植的实验研究   总被引:1,自引:0,他引:1  
目的 研究在亚低温环境中实施干细胞移植的可行性,为创伤性脑损伤(traumatic brain injuries,TBI)患者接受亚低温治疗期间实施干细胞移植提供实验依据.方法 利用温度敏感型猿猴病毒40大T抗原(tsSV40LT)建立温度敏感型人源性脐带间充质干细胞系(tsUCMSOs),观察其在亚低温(33℃)和正常体温(37℃)下细胞形态、核增殖指数(PIx)及端粒酶活性的变化;建立小鼠TBI亚低温治疗模型,在创伤灶周围半损伤带移植tsUCMSCs,检测其存活率、增殖和凋亡指数,并进行神经功能缺陷评分.结果 tsUCMSCs在33℃培养时,胞体呈长梭形,折光性强,增殖指数和端粒酶活性均较高,但在37℃时胞体扁平,折光性差,细胞老化明显,增值指数和端粒酶活性均明显降低.移植于创伤灶周围半损伤带的tsUCMSCs较对照组(非温度敏感型UCMSCs移植组)细胞存活率明显增高(P<0.05),细胞核增殖抗原高表达,凋亡细胞少见,小鼠神经功能明显好转(P<0.05).结论 tsUCMSCs的建立使TBI亚低温治疗期间实施干细胞移植成为可能,为未来脑创伤的救治提供了新的方法.  相似文献   

15.
目的 研究大鼠脊髓损伤后胚胎脊髓(FSC)移植是否能够影响胶质纤维酸性蛋白(GFAP)的表达和伤后大鼠后肢功能的恢复情况。方法 将60只大鼠分为脊髓半脊髓半切洞损伤_胚胎脊髓移植组(A组)和单纯脊髓半切洞损伤组(B组)。伤后1,3,,7,14,28天,应用行为学和电生理检查观察大鼠功能恢复情况,应用原位杂我和免疫细胞化学方法观察GFAP的表达,并采用计算机图像分析技术,进行定量分析。结果 大鼠脊髓  相似文献   

16.
目的探讨局灶性脑梗死后细胞周期调控对星形胶质细胞增殖的影响。方法光化学方法制作大鼠缺血模型,腹腔注射细胞周期抑制剂Olomoucine进行干预。应用免疫组织化学法观察缺血后30d假手术组、对照缺血组和干预组(按8mg/kg给予Olomoucine)损伤侧皮层病灶周围胶质纤维酸性蛋白(glial fibriliary acidic proten,GFAP)阳性表达;免疫印迹法(Westem blot)观察GFAP和增殖细胞核抗原(proliferation cell nuclear antigen,PCNA)蛋白的表达;半定量逆转录一聚合酶链反应法(RT-PCR)观察GFAP mRNA的表达;HE染色测定皮层中风囊的体积。结果缺血后30d缺血组损伤侧皮质有明显的中风囊,形成胶质瘢痕,且周围胶质细胞增殖、活化呈密集型改变;对照组GFAP mRNA的表达最明显(P〈0.05);干预组损伤侧皮质中风囊体积明显减小(P〈0.05),胶质细胞增殖明显受到抑制(P〈0.05),且GFAP和PCNA蛋白表达明显减弱(P〈0.05)。结论细胞周期调控可部分抑制胶质细胞的活化、增殖及瘢痕的形成。  相似文献   

17.
目的 研究腺病毒介导的脑源性神经营养因子(BDNF)基因转移对脑损伤后细胞凋亡的影响。方法 将重组腺病毒载体4μl注入承受单侧大脑皮质重锤打击伤的海马区,对照组注射病毒缓冲液。伤后3h,1,3,7,14d利用免疫组化单标和(或)双档染色、原位杂交-免疫组化双标染色、DNA末端原位标记以及流式细胞仪等方法,检测伤侧大脑皮质、海马区BDNF及凋亡相关信号表达的改变。结果 与对照组相比,注射病毒载体组动物术后3,7d海马CA1、CA3区BDNF神经元显著增多,而凋亡细胞显著减少(P<0.01);表达BDNF的神经元较少并同时表达凋亡相关信号。结论 腺病毒介导的BDNF基因转移对海马神经元具有保护作用。  相似文献   

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