Relation between plasma brain-derived neurotrophic factor and nerve growth factor in the male patients with alcohol dependence

Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are thought to be related to neuroprotection in cell culture and animal studies. Our aim was to verify the changes in human plasma BDNF and NGF concentrations induced by chronic alcohol use. Forty-one male patients with alcohol dependence were sampled the next morning of admission and compared with 41 healthy male subjects. Plasma BDNF and NGF were assayed using an enzyme-linked immunosorbent assay (ELISA). Mean plasma BDNF level was significantly higher in the patients with alcohol dependence (3502.21 ± 1726.9 pg/mL) compared with the healthy subjects (861.75 ± 478.9 pg/mL) (P = .000). Mean plasma NGF level was also significantly higher in patients with alcohol dependence (137.64 ± 32.7 pg/mL) than in healthy subjects (112.61 ± 90.2 pg/mL) (P = .012). Plasma BDNF and NGF levels showed significant negative correlation in alcohol dependence group (r = −0.388, P = .012). Increased plasma BDNF and NGF with negative correlation in alcohol-dependent patients may have some role in the regeneration of damage done by chronic alcohol use.     

鼠源性神经生长因子对正己烷中毒患者内源性神经生长因子水平影响

目的 探讨鼠源性神经生长因子(mNGF)治疗对正己烷中毒患者内源性神经生长因子(NGF)水平的影响.方法 9例正己烷中毒患者(病例组)经mNGF治疗1、6及12个月后,分别检测血清内源性NGF水平,并与正常对照人群(对照组)比较.结果 病例组3次检测血清内源性NGF水平均低于检出限值(30 ng/L),检出率为0％,对照组血清内源性NGF检出率为35.7％.mNGF治疗1年后,病例组周围神经异常表现均有显著改善.结论 正己烷中毒患者血清内源性NGF水平较低;mNGF能显著改善患者的周围神经异常表现;血清内源性NGF水平恢复晚于神经行为异常的恢复,恢复到正常水平可能需要较长时间.     

丁苯酞对脑梗死患者脑源性神经营养因子的影响

目的:探讨丁苯酞对急性脑梗死患者血清脑源性神经营养因子(BDNF)水平和神经功能的影响.方法:60例急性脑梗死患者随机分为对照组(n=30)和治疗组(n=30),所有患者根据缺血性卒中诊治指南给予规定药物,治疗组加用丁苯酞.在治疗前以及治疗2周和6周时检测血清BDNF水平,采用NIHSS评定神经功能缺损程度.结果:治疗组治疗2周(P=0.045)和治疗6周时(P=0.034) NIHSS评分均显著性低于对照组.两组治疗后血清BDNF水平均显著性增高,治疗组血清BDNF水平在治疗2周时(P=0.015)和6周时(P=0.021)均显著高于对照组.血清BDNF水平与NIHSS(r=-0.705,P＜0.001)呈显著性负相关.结论:丁苯酞治疗急性脑梗死能更有效地促进神经功能恢复,其机制可能与提高血清BDNF水平相关.     

High-dose dietary supplementation of vitamin A induces brain-derived neurotrophic factor and nerve growth factor production in mice with simultaneous deficiency of vitamin A and zinc

Marginal vitamin A and zinc (Zn) deficiency often co-exist in many populations. Vitamin A plays a trophic role in brain and is important for its development. We investigated effects of dietary supplementation of vitamin A on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) production in mice depleted for vitamin A and Zn. After 3 months' feeding with a low vitamin A and Zn (LVA-LZ) diet, mice were divided into two groups and replenished with either normal or high vitamin A with low Zn diet for an additional 2 months. Levels of BDNF and NGF were measured from extracts of hippocampus, cortex and cerebellum at the end of the third and fifth months. The LVA-LZ group tended to show decreased amounts of the BDNF and NGF, while animals supplemented with high vitamin A along with Zn deficiency had high BDNF and NGF concentrations. From these results, we conclude that vitamin A may increase BDNF and NGF levels.     

High-dose dietary supplementation of vitamin A induces brain-derived neurotrophic factor and nerve growth factor production in mice with simultaneous deficiency of vitamin A and zinc

Abstract

Marginal vitamin A and zinc (Zn) deficiency often co-exist in many populations. Vitamin A plays a trophic role in brain and is important for its development. We investigated effects of dietary supplementation of vitamin A on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) production in mice depleted for vitamin A and Zn. After 3 months' feeding with a low vitamin A and Zn (LVA-LZ) diet, mice were divided into two groups and replenished with either normal or high vitamin A with low Zn diet for an additional 2 months. Levels of BDNF and NGF were measured from extracts of hippocampus, cortex and cerebellum at the end of the third and fifth months. The LVA-LZ group tended to show decreased amounts of the BDNF and NGF, while animals supplemented with high vitamin A along with Zn deficiency had high BDNF and NGF concentrations. From these results, we conclude that vitamin A may increase BDNF and NGF levels.     

血液脑源性神经营养因子水平与阿尔茨海默病关系的Meta分析

目的探讨阿尔茨海默病(Alzheimer disease,AD)患者血液脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)水平变化情况。方法检索中国知网、万方、维普数据库、中国生物医学文献数据库、Pub Med、西文生物数据库有关AD患者血液BDNF变化的病例对照研究。检索年限均为建库以来至2016年5月。采用纽卡斯尔渥太华量表(Newcastle Ottawa scale,NOS)标准文献质量进行评价。用Stata12.0软件进行Meta分析,检验水准为α=0.05。结果总计11篇文献纳入本次研究,其中英文文献7篇,中文文献4篇。NOS评分7~8分。病例组血液BDNF水平低于对照组,两组比较差异有统计学意义(Z=2.331,P=0.020)。年龄、地区为可能异质性因素。以病例组中位年龄73.2岁为分界线,结果表明年龄较大组,AD患者血液BDNF水平与正常对照组比较差异有统计学意义(P0.05);年龄较小组与正常对照组比较差异无统计学意义(P0.05)。以是否为亚洲人群进行分析,结果表明尚不能认为亚洲人群病例组血液BDNF水平与正常对照组比较差异有统计学意义(P0.05),而非亚洲人群两组BDNF水平比较差异有统计学意义(P0.05)。固定效应模型和随机效应模型计算结果趋向一致,提示合并结果可靠。用Begg’s test检验漏斗图对称性研究没有明显的发表偏倚存在。结论血液BDNF水平下降可能与AD的发生有关。     

Nerve growth factor and brain-derived neurotrophic factor: a possible etiopathogenic role in sensorineural hearing loss. Preliminary data

Nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) are members of a family of structurally related secreted proteins, termed neurotrophins, which promote and regulate the survival of many kinds of neurons in the peripheral nervous system. Aim of the study is to dose the serum level of NGF and BDNF in 8 patients affected by sensorineural hearing loss (SNHL). The results show that in these patients the amount of circulating NGF, but not of BDNF, is significantly lower in comparison to that found in age-matched controls. The preliminary data of the present study suggest that NGF might have a crucial role in the auditory pathway, promoting the survival and preventing the degeneration of sensorineural cells.     

血液脑源性神经营养因子水平与强迫症关系的Meta分析

目的综合分析血液脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)水平与强迫症(obsessivecompulsive disorder,OCD)的关系。方法在万方、中国知网及Pub Med中检索,入选关于血液BDNF水平与OCD关系的病例对照研究,采用Stata12.0软件对数据进行Meta分析,P0.05为差异有统计学意义。结果共有7篇文献纳入分析,获得样本543例,病例组308例,对照组235例。Meta分析结果显示,OCD患者血液BDNF水平低于对照组(合并效应值SMD=-1.466,95%CI为-2.346~-0.585,P0.05)。敏感性分析显示,两组在血液BDNF水平上的差异结果可靠。Bgger检验显示无明显的发表偏倚。结论血液BDNF水平下降可能与OCD的发生有关。     

Alterations of serum brain-derived neurotrophic factor levels in early alcohol withdrawal

AIMS: Alcohol withdrawal-enhanced neurotoxicity contributes to the addictive process. Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal plasticity and learning. In this study, we explored the changes of serum BDNF levels in alcoholic patients at baseline and after one-week alcohol withdrawal. METHODS: Twenty-five alcoholic patients were admitted for alcohol detoxification treatment, and 22 healthy control subjects were also enrolled. We collected blood samples of the patient group on the first and seventh day of alcohol withdrawal, and measured serum BDNF level with sandwich enzyme-linked immunosorbent assay. The severity of withdrawal symptoms was evaluated by the Clinical Institute Withdrawal Assessment-Alcohol, Revised every eight hours. RESULTS: Serum BDNF levels did not differ significantly between alcoholic patients and control subjects. But BDNF levels were found to be significantly increased one week after alcohol withdrawal (from 13.9 +/- 3.8 ng/ml to 15.4 +/- 3.8 ng/ml, P = 0.03). A significant positive correlation was found between baseline BDNF level and baseline withdrawal severity (r = 0.45, P = 0.03). CONCLUSIONS: The present study suggests that elevated serum BDNF levels were found in early alcohol withdrawal, implying that BDNF may involve in neuroadaptation during the period.     

脑源性神经营养因子预处理对大鼠脑缺血再灌注损伤氧化应激及神经细胞凋亡的影响

目的探讨不同剂量的脑源性神经营养因子（BDNF）预处理对大鼠局灶性脑缺血再灌注（I／R）损伤氧化应激及神经细胞凋亡的影响。方法采用大鼠大脑中动脉线栓法（MCAO）建立局灶性脑I／R损伤模型,BDNF于缺血前12h经侧脑室注射给药。采用黄嘌呤氧化酶法和硫代巴比妥酸法检测脑组织超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量,TUNEL法检测脑皮层凋亡神经细胞,免疫组化法检测Bcl-2、Bax蛋白表达。结果与I／R组比较,BDNF预处理各组脑组织SOD活性明显增强,MDA含量明显降低,给药各组中脑皮层Bcl-2蛋白表达明显增高,而Bax蛋白表达及TUNEL阳性细胞指数均明显降低（P〈0．01）;在BD-NF预处理各组中,以BDNF预处理高剂量组脑组织SOD活性及Bcl-2蛋白表达最高、MDA含量和Bax蛋白的表达以及TUNEL阳性细胞指数最低（P〈0．01）。结论不同剂量的BDNF预处理均能明显减轻脑I／R后氧化应激和神经细胞凋亡,具有不同程度的脑保护作用,其保护作用与BDNF预处理的剂量有关。其机制可能与BDNF预处理能够提高机体内源性抗氧化物质的含量及调节凋亡相关基因的不同表达有关。     

The role of brain-derived neurotrophic factor in the pathophysiology of adolescent suicidal behavior

Adolescent suicide research has mostly focused on demographic risk factors. Such studies focus on who is at risk, but do not explain why certain adolescents are at risk for suicide. Studies of the neurobiology of adolescent suicide could clarify why some youths are more suicidal than others and help to find biological markers of suicidal behavior in teenagers. Over the past decade the role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of suicidal behavior has attracted significant attention of scientists. BDNF is involved in the pathophysiology of many psychiatric disorders associated with suicidal behavior including depression, post-traumatic stress disorder, schizophrenia, and obsessive-compulsive disorder. BDNF dysregulation could be associated with increased suicidality independently of psychiatric diagnoses. BDNF plays an important role in the regulation and growth of neurons during childhood and adolescence. Prominent among the brain regions undergoing developmental change during adolescence are stressor-sensitive areas. The serotonin dysfunction found in adolescent and adult suicidal behavior could be related to the low level of BDNF, which impedes the normal development of serotonin neurons during brain development. BDNF dysfunction could play a more significant role in the pathophysiology of psychiatric disorders and suicidal behavior in adolescents than in adults. Treatment-induced enhancement in the BDNF function could reduce suicidal behavior secondary to the improvement in psychiatric pathology or independently of improvement in psychiatric disorders. It is interesting to hypothesize that BDNF could be a biological marker of suicidal behavior in adolescents or in certain adolescent populations.     

The effects of perinatal protein malnutrition on spatial learning and memory behaviour and brain-derived neurotrophic factor concentration in the brain tissue in young rats

This study aimed to investigate the effects of perinatal protein malnutrition on brain derived-neurotrophic factor (BDNF) concentration in brain tissue and spatial learning and memory performance in young rats. Nine pregnant Wistar rats were assigned into three groups. Rats in one group were fed with a control diet containing 20% protein. Rats in remaining two groups were fed with a diet containing 6% protein from gestation day eight and day 15 respectively till four weeks after birth. At four weeks of age, the rat pups were evaluated for spatial learning ability using Morris Water Maze (MWM) task. At the end of the behaviour tests, rat pups were sacrificed and the brain tissue samples were collected for measurement of total protein and BDNF concentrations. It was found that rat pups fed the low protein diet had lower body weight and slightly lighter brain compared to the control pups. Total protein levels in hippocampus and cerebral cortex were significantly lower in malnourished pups than the controls. The concentration of BDNF in the hippocampus was also significantly lower in rat pups suffered protein malnutrition from early pregnancy than in the controls. MWM tests showed that perinatal protein deprivation, particularly from early pregnancy, significantly impaired learning and memory ability. The results of the present study indicate that perinatal protein malnutrition had adverse influence on spatial navigation and brain BDNF levels in rats. The decreased hippocampal BDNF concentration might partially contribute to the poor learning memory performance in the protein deprived rats.     

三磷酸胞苷对脑缺血大鼠脑源性神经营养因子的影响

目的:观察CTP对局灶脑缺血大鼠BANF表达的影响.方法:应用免疫组化方法观察不同缺血时间CTP治疗组及脑缺血组BDNF阳性细胞数,并进行图像分析.结果:CTP组及缺血组BDNF两组细胞形态无明显不同,但CTP治疗组阳性细胞数显著高于相应缺血对照组.结论:三磷酸胞苷可提高大鼠局灶脑缺血半暗带区BDNF的表达水平.     

Molecular mechanisms of cognitive impairment in iron deficiency: Alterations in brain-derived neurotrophic factor and Insulin-like growth factor expression and function in the central nervous system

Objective

The present review examines the relationship between iron deficiency and central nervous system (CNS) development and cognitive impairment, focusing on the cellular and molecular mechanisms related to the expression and function of growth factors, particularly the insulin-like growth factors I and II (IGF-I/II) and brain-derived neurotrophic factor (BDNF), in the CNS.

Methods

Nutritional deficiencies are important determinants in human cognitive impairment. Among these, iron deficiency has the highest prevalence worldwide. Although this ailment is known to induce psychomotor deficits during development, the precise molecular and cellular mechanisms underlying these alterations have not been properly elucidated. This review summarizes the available information on the effect of iron deficiency on the expression and function of growth factors in the CNS, with an emphasis on IGF-I/II and BDNF.

Results and discussion

Recent studies have shown that specific growth factors, such as IGF-I/II and BDNF, have an essential role in cognition, particularly in processes involving learning and memory, by the activation of intracellular-signaling pathways involved in cell proliferation, differentiation, and survival. It is known that nutritional deficiencies promote reductions in systemic and CNS concentrations of growth factors, and that altered expression of these molecules and their receptors in the CNS leads to psychomotor and developmental deficits. Iron deficiency may induce these deficits by decreasing the expression and function of IGF-I/II and BDNF in specific areas of the brain.     

母鼠慢性不可预见性应激后对子代大鼠海马脑源性神经营养因子表达的影响

【目的】探讨母鼠接受慢性不可预见性应激(chronic unpredictable stress,CUS)后短期内受孕对1月龄子代大鼠大脑海马中脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的影响。【方法】SD系成年雌性大鼠随机分为正常对照母鼠组(8只)和CUS母鼠组(12只)。采用11种刺激方法对CUS母鼠组进行21 d慢性不可预见性应激。于应激前、后,两组母鼠进行开场试验及蔗糖水消耗试验,分析CUS对母鼠自主行为的影响。用免疫组织化学染色和实时聚合酶链反应(Realtime Polymerase Chain Reaction,RT-PCR)法检测1周内受孕的CUS母鼠组所得子代大鼠(雌雄各30只)1月龄时海马中BDNF的表达情况,并与同期受孕的正常对照母鼠组所产子代大鼠进行同性别间的比较。【结果】CUS母鼠组应激后开场试验的总路程、周边路程、中央路程和蔗糖水消耗试验的蔗糖水消耗量明显少于应激前及正常对照母鼠组。子代大鼠海马中BDNF免疫反应阳性细胞的相对灰度值在正常雌性子代组为42.4±6.9,CUS雌性子代组为36.1±8.5(P0.05);在正常雄性子代组为43.7±6.4,CUS雄性子代组为39.6±8.4(P0.05)。子代大鼠海马中BDNF mRNA的表达量在正常雌性子代组为6.65±0.26,CUS雌性子代组为4.55±0.37(P0.05);在正常雄性子代组为6.77±0.20,CUS雄性子代组为4.75±0.30(P0.05)。【结论】母鼠接受慢性不可预见性应激后短期内受孕,会使子代大鼠海马中BDNF mRNA转录水平显著下降,而且这种改变与BDNF阳性细胞在海马中表达减少一致。     

鼠神经生长因子治疗带状疱疹的临床研究

目的 观察鼠神经生长因子(mNGF)治疗带状疱疹的临床疗效.方法 将64例带状疱疹患者,按随机数字表法分为治疗组和对照组,每组32例,两组均给予常规治疗,治疗组在常规治疗的基础上应用mNGF肌肉注射,每日30 μg,共14d,每5d观察疼痛变化情况,共观察1个月.结果 治疗组疼痛减轻时间、疼痛消失时间分别为(4.36±2.01)、(12.29±1.98)d,均短于对照组的(7.23±3.57)、(20.36±2.24)d,差异有统计学意义(t=5.21、8.37,P＜0.01);治疗组总有效率为96.9％(31/32),显著高于对照组的71.9％(23/32),差异有统计学意义(P＜0.05).结论 mNGF配合常规治疗能明显缩短带状疱疹受累神经的修复过程,改善临床症状,并且不良反应少.     

铅对大鼠脑组织脑源性神经生长因子及其受体P75NTR表达的影响

目的 研究醋酸铅对大鼠脑组织神经生长因子(BDNF)及其受体P75NTR表达的影响.方法 将雌雄各半的健康成年SD大鼠48只随机分为1个对照组和3个染铅组,每组12只.染铅组分别用25、50、100mg/kg的醋酸铅处理SD大鼠,腹腔注射5 d,于第6天取材,用石墨炉原子吸收法测定大鼠血清和脑组织中的铅含量;逆转录聚合酶链反应(RT-PCR)和免疫组化方法测定脑组织中BDNF mRNA和蛋白的表达;免疫组化测定脑组织中P75NTR的表达.结果 大鼠血清和脑组织中铅含量迅速增加,与对照组比较,差异有统计学意义(P＜0.01,P＜0.05);RT-PCR结果表明,50、100mg/kg剂量组BDNF mRNA表达在皮层(0.72±0.09,0.77±0.05)与海马组织(0.77±0.10,0.92±0.08)中明显增加,与对照组(0.52±0.05,0.33±0.03)比较,差异有统计学意义(P＜0.05);免疫组化分析表明,各剂量组皮层组织BDNF面密度明显增高,平均灰度明显低于对照组,海马部位与对照组比较,各剂量组BDNF面密度明显增加,差异均有统计学意义(P＜0.01),50、100mg/kg组平均灰度明显下降,与对照组的差异有统计学意义(P＜0.01);对照组和25 mg/kg组未见P75NTR阳性表达,50、100mg/kg组可见P75NTR阳性表达.结论 醋酸铅可以诱导大鼠大脑皮层、海马组织中BDNF和P75NTR的表达,该诱导作用可能在其神经损伤修复中有重要意义.     

虾青素对糖尿病大鼠海马脑源性神经营养因子表达的影响

目的探讨虾青素对糖尿病大鼠海马脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的影响。方法腹腔注射链脲佐菌素建立糖尿病大鼠模型,造模成功后,分为模型组、阳性对照组和虾青素组。阳性对照组和虾青素组分别灌胃盐酸二甲双胍和虾青素溶液。正常组灌胃等量生理盐水。药物干预6周后,分别对各组大鼠进行Morris水迷宫实验,采用real-time PCR法和ELISA法分别检测海马BDNF的表达和含量。多个样本均数比较采用单因素方差分析,两两比较采用LSD法,P0.05为差异有统计学意义。结果四组大鼠的平台象限路径百分比和平台象限停留时间[(0.615 7±0.042)、(0.321 5±0.020)、(0.533 6±0.027)、(0.498 6±0.029)%与(43.37±6.98)、(21.46±5.65)、(36.64±5.87)、(33.18±6.35)s]比较,差异均有统计学意义(均P0.05)。两两比较发现,与正常组相比,模型组大鼠在平台象限路径百分比和平台象限停留时间均显著减少,差异均有统计学意义(均P0.05)。与模型组相比,阳性对照组和虾青素组在平台象限路径百分比和平台象限停留时间明显提高,差异均有统计学意义(均P0.05)。四组大鼠BDNF含量[(5.38±0.96)、(1.72±0.33)、(3.54±0.62)、(3.17±0.57)pg/ml]比较,差异有统计学意义(P0.05),与正常组比较,模型组BDNF的含量降低了68.03%,差异有统计学意义(P0.05)。四组大鼠BDNF m RNA相对表达量[(0.98±0.17)、(0.53±0.10)、(0.74±0.11)、(0.75±0.12)]比较,差异有统计学意义(P0.05),模型组BDNF的m RNA水平与正常组相比降低了45.92%,差异有统计学意义(P0.05)。结论虾青素具有提高糖尿病大鼠认知功能的作用,其机制可能与上调BDNF的表达有关。     

Decreased plasma brain-derived neurotrophic factor levels in institutionalized elderly with depressive disorder

ObjectivesTo compare the differences in plasma brain-derived neurotrophic factor (BDNF) levels among institutionalized ethnic Chinese elderly participants with major depression, those with subclinical depression, and a nondepressed control group.DesignA cross-sectional study.SettingThe veterans' home in southern Taiwan.ParticipantsOne hundred sixty-seven residents.MeasurementsQuestionnaires including the Minimum Data Set Nursing Home 2.1, Chinese-language version, and the short-form Geriatric Depression Scale, Chinese-language version. Depressive disorder was diagnosed by a well-trained psychiatrist using DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision) criteria. We measured plasma BDNF levels in the following 3 groups: nondepressive subjects (n = 122), subclinically depressive subjects (n = 33), and subjects with major depression (n = 12). Plasma BDNF was assayed using the sandwich ELISA method.ResultsWe noted a significantly negative association between age and plasma BDNF in the regression model. There was no significant correlation between BDNF plasma levels and body weight or platelet counts. We found that plasma BDNF was significantly lower in the major depressive group (mean, 115.1 pg/mL; SD, 57.2) than in the nondepressive group (mean, 548.8 pg/mL; SD, 370.6; P < .001). The BDNF plasma concentrations in the subclinically depressive group (mean, 231.8 pg/mL; SD, 92.4; P < .001) and control group were also significantly different.ConclusionsOur findings revealed that plasma BDNF levels were reduced not only in ethnic Chinese elderly patients with major depressive disorder but also in those with subclinical depression. This makes the plasma BDNF level a potential biological marker for clinical or subclinical depression.     

脑源性神经营养因子对皮质酮诱导新生大鼠海马神经元凋亡的保护作用

目的 探讨脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)对皮质酮诱导新生大鼠海马神经元凋亡的保护作用。 方法 原代培养新生大鼠海马神经元,并分成对照组、皮质酮组、皮质酮+BDNF组,皮质酮造模浓度为100 μM,分别采用浓度为0.1、1、10、25、50、100 ng/ml的BDNF干预,造模及干预时间均为24 h。CCK8法测定细胞活力,分析BDNF的最佳作用浓度,流式细胞术和 Hoechst荧光染色检测细胞的凋亡情况,免疫印迹(Western-blotting)法检测细胞Caspase-3、Caspase-9的表达水平。 结果 与对照组比较,皮质酮组神经元凋亡率由(10.7±1.2)%上升为(33.9±3.5)%(t=18.707,P<0.01),胞体透亮,部分细胞核碎裂,凋亡特征明显,Caspase-3、Caspase-9表达显著上调(t₁=27.098,P₁＜0.01;t₂=24.311,P₂＜0.01);BDNF作用后,细胞活力显著上升,在浓度为1 ng/ml时与皮质酮组比较差异有统计学意义(t=3.562,P＜0.05),分析得出BDNF最佳浓度为48 ng/ml;BDNF(48 ng/ml)干预完成后,细胞凋亡率较皮质酮组下降至(18.7±2.1)%,差异有统计学意义(t=11.478,P＜0.01),细胞形态基本恢复正常,Caspase-3、Caspase-9表达明显下调(t₁=17.341,P₁=0.002;t₂=14.993,P₂=0.005)。 结论 BDNF能有效拮抗皮质酮诱导的海马神经元凋亡,保护神经元细胞。