Ginkgo biloba extract (EGb 761) as an antioxidant factor of exogenous origin

Extracted from Ginkgo biloba leaves, the EGb 761 has a great number of therapeutical properties and anti-stress effects, for example the antioxidant one. We estimated in our experiment the influence of a chronic treatment with EGb 761 on the concentration of the main product of lipidic degradation--malondialdehyde (MDA), in cerebral cortex, in diencephalon, thymus and gastric mucosa. The experiment was performed on Wistar rats, male, young. The MDA estimation was performed by the spectrocalorimetry. We have determined that the stress raised the MDA concentration in all examined structures with approximately 100% and 80% of animals manifested stress ulcer. The treatment with EGb 761 before a stress inhibits the post-stress growth of MDA concentration and the process of stress ulcer formation.     

EGb761对急性大鼠脊髓损伤后血脊髓屏障的保护作用及其机制研究

[目的]观察银杏叶提取物(EGb761)对急性大鼠脊髓损伤后炎症反应及血脊髓屏障的保护作用,探讨其对急性脊髓损伤的作用机制.[方法]120只雌性SD大鼠,体重200～220 g,随机分为假手术组(A组)、损伤对照组(B组)、EGb761治疗组(C组),每组40只.A组仅行T9椎板切除术,不致伤脊髓.B、C组用改良Allen's法以25gcf致伤力制作大鼠T9脊髓损伤模型,C组术后至处死前每日经腹腔给予EGb761 100 mg/kg(首次给药在术后30min),A、B组在同一时间给予等量生理盐水.术后3、6、24、72 h分批处死动物,以T9为中心取损伤节段脊髓,采用Evans蓝含量测定法观察SCI后血脊髓屏障(blood cerebrospinal barrier,BSCB)通透性的变化,采用ELISA法测定脊髓组织白介素-1β(interleukin-1β,IL-1β)的含量,免疫组织化学方法检测细胞间粘附分子-1(intercellular adhesion molecular-1,ICAM-1)在脊髓组织中的表达变化.[结果]A组各时间点脊髓中无明显Evan's蓝渗漏,IL-1β含量及ICAM-1表达维持在基础水平;B组各时间点Evan's蓝渗漏、IL-1β含量及ICAM-1表达量均明显高于A组;C组EGb761干预后在6、24、72 h时Evan's蓝通过BSCB漏入脊髓组织量显著低于B组,在各时间点IL-1β、ICAM-1的表达均较B组明显减少.[结论]在Allen's大鼠急性脊髓损伤模型中,EGb761能降低局部脊髓中IL-1β含量,下调ICAM-1的表达,减轻BSCB的破坏.     

Ginkgo biloba (EGb 761) usage attenuates testicular injury induced by testicular ischemia/reperfusion in rats

Introduction  We investigated the effect of ginkgo biloba on testicular ischemia-reperfusion (IR) injury. Materials and methods  Thirty-two Wistar Albino rats were randomly assigned into four groups. Torsion/detorsion (T/D) performed to the rats in group 1, group 2 received ginkgo biloba (50 mg/day) for a month before T/D, group 3 received only gingko biloba (50 mg/day) for a month and group 4 was defined as sham group. After 1 month the testes were removed. Results  Mean testicular malondialdehyde, nitrate and nitrite levels were significantly increased in group 1 compared to groups 2, 3 and 4 (P < 0.05). The rats in group 3 provided basal histological appearance. In group 1, edema, congestion and hemorrhage between seminiferous tubules were predominant. In group 2, histopathologic features were markedly less than group 1. Conclusions  Malondialdehyde, nitrate and nitrite levels were increased after unilateral testicular torsion. EGb 761 has a protective effect on testicular injury induced by IR.     

The effects of gingko biloba extract (EGb 761) on experimental acute pancreatitis

BACKGROUND AND OBJECTIVE: Acute pancreatitis is an important and fatal disease with high mortality and morbidity. Although the pathogenesis of acute pancreatitis is poorly understood, there are many studies that suggest the role for oxygen free radicals (OFRs) in the development of pancreatitis and its complications and show beneficial effects of scavenger treatment. In the present study, we aimed to investigate whether Egb761, the standardized extract of gingko biloba, restrains the generation of OFRs and ameliorates the histopathologic findings of acute pancreatitis. MATERIALS AND METHODS: Sixty male Sprague Dawley rats were randomly assigned to one of the following experimental groups. In early and late pancreatitis and treatment groups, acute pancreatitis was induced by retrograde infusion of 3% sodium taurocholate. In treatment groups, 100 mg/kg Egb 761 was given intraperitoneally (IP) 24 h and immediately before induction of pancreatitis. Sham-operated rats received isotonic saline instead of sodium taurocholate. After observation times of 3.5 and 12 h, the pancreas was removed for light microscopy and determination of malondialdehyde (MDA) levels as a marker for OFRs-induced lipid peroxidation. Serum samples also were obtained for amylase and lipase levels. RESULTS: There was no significant difference in control and sham-operated groups in terms of histopathologic findings and serum enzyme levels. The tissue concentrations of MDA and serum enzyme levels were significantly elevated in early and late treatment groups as compared with the control group. The treatment with Egb 761 caused significant decrease in serum amylase and lipase levels and histopathologic scores as compared with early and late pancreatitis groups. CONCLUSIONS: Prophylactic application of Egb761 exerts highly beneficial influence on the course of acute pancreatitis, and this seems to be related to the oxygen radical scavenger effect of Egb761.     

Protective effects of Ginkgo biloba extract in rats with hypoxia/reoxygenation-induced intestinal injury

Background

The purpose of this study is to investigate the protective effects of Ginkgo biloba extract (EGb 761) in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury.

Methods

One-day-old Wistar albino rat pups (n = 21) were randomly divided into 3 groups: group 1 (control, untreated and not exposed to H/R, n = 7), group 2 (untreated but exposed to H/R, n = 7), and group 3 (EGb 761 + H/R, n = 7). Ginkgo biloba extract was administered (100 mg/kg per day, subcutaneously) to group 3 for 3 days. On the fourth day, all animals except controls were exposed to H/R and were killed 6 hours after H/R. Histopathologic injury scores (HIS), malondialdehyde, glutathione (GSH), GSH-peroxidase (Px) activities, and nitric oxide (NO) levels were measured on intestinal samples.

Results

Although the control group had normal HIS, group 2 had grade 3 HIS. In contrast, group 3 had minimal HIS, and these results were significantly better than those of group 2 (P < .001). Malondialdehyde and NO levels of group 3 were significantly lower than those of group 2 (P < .01). Glutathione and GSH-Px activities of group 1 were higher than those of groups 2 and 3 (P < .05). However, there were no significant differences for GSH and GSH-Px activities between groups 2 and 3.

Conclusions

This study showed that hypoxia and NO contributed to the pathogenesis of H/R-induced intestinal injury and that prophylactically administered EGb 761 had a protective effect on bowel injury.     

银杏叶提取物(EGb50)对大鼠坐骨神经再生的影响及其量效关系

目的 评价银杏酮酯(EGb50)对大鼠坐骨神经损伤后神经再生的影响及其量效关系.方法 建立大鼠坐骨神经损伤模型,将雄性SD大鼠96只随机分为4组损伤对照组、银杏酮酯高剂量组(200 mg·kg-1·d-1)、银杏酮酯中剂量组(100mg·kg-1·d-1)、银杏酮酯低剂量组(50 mg·kg-1·d-1).分别于术后2、4、6、8周用电生理学、组织学和功能测定评估坐骨神经再生和功能恢复情况.结果 术后坐骨神经功能指数(SFI)、小腿三头肌肌张力、运动神经传导速度、小腿三头肌肌细胞截面积恢复率及有髓神经纤维通过率在各时间点上银杏酮酯各剂量组均优于对照组(P＜0.01).除坐骨神经功能指数外,其它各项指标银杏酮酯高剂量组均优于中低剂量组(P＜0.01,P＜0.05).结论 银杏酮酯可以促进损伤神经的再生,且对神经再生的促进作用存在一定的量效关系.     

银杏叶提取物对黄曲霉毒素B_1诱导的大鼠肝癌的化学预防作用

目的 探讨银杏叶提取物(EGb761)对黄曲霉毒素B_1(AFB_1)致大鼠肝癌(HCC)发生发展的干预作用及其机制.方法 A组(AFB_1组28只)、B组(AFB_1+EGb761组29只)和C组(对照组14只)3组大鼠,定期肝活检并于第64周全部处死,观察实验肝癌发生过程中大鼠肝组织病理学、肝癌发生率、丙二醛(MDA)及8-羟基鸟嘌呤核苷(8-OHdG)蛋白表达的变化.结果 B组大鼠诱癌各时期肝脏损害均较A组轻,增生性病变发生亦较迟,肝癌诱发率(26.92%)明显低于A组(76.00%)(P<0.01),对照组无肿瘤发生.在各检测点(实验第14、28、42、64周),B组大鼠肝组织MDA含量(nmoL/mg蛋白)分别为0.14±0.01、0.24±0.01、0.36±0.01、0.60±0.01,均显著低于A组的0.27±0.01、0.66±0.01、0.56±0.01、0.93±0.02(P<0.05),在第64周时还明显低于C组的0.84±0.03(P<0.05);B组在第28、42和64周时8-OHdG蛋白的表达强度均显著低于A组(P<0.05).结论 EGb761能够明显抑制AFB_1诱发大鼠肝癌的发生,这可能与其降低了自由基所致的脂质过氧化反应、减轻AFB_1诱导的氧化损伤有关.     

Effects of mexiletine,ginkgo biloba extract (EGb 761), and their combination on experimental head injury

Lipid peroxidation (LP) and brain edema are important factors that produce tissue damage in head injury. The purpose of this study was to investigate the effect of mexiletine, gingko biloba extract (EGb 761), and their combination on LP and edema after moderate head trauma. Forty rats were randomly and blindly divided into four groups of ten animals each: control group (bolus injection of physiological saline), mexiletine group (50 mg/kg per injection), EGb 761 group (30 mg/kg per injection), and mexiletine plus EGb 761 group (50 mg/kg and 30 mg/kg per injection, respectively). The injections were given intraperitoneally at 1 h, 9 h, and 17 h after trauma. Twenty-four hours after injury, the rats were killed, and malondialdehyde (MDA) levels and brain water content were determined. Rats treated with mexiletine, EGb 761, and mexiletine plus EGb 761 had significantly lower MDA levels than the control group (P<0.01). The lowest MDA levels were measured in the mexiletine plus EGb 761 group. However, there was no significant difference in brain water content between treated groups and the control group (P>0.05). These findings show the usefulness of mexiletine and its combination with EGb 761 as a cerebroprotective agent in this model of experimental head injury.     

银杏叶提取物对实验性脊髓损伤后诱导型一氧化氮合成酶表达的影响

[目的]观察提取物(EGb)对脊髓损伤后诱导型一氧化氮合酶(iNOS)的影响.[方法]SD雄性大鼠(SPF级)30只,体重250～300 g,随机分成2组,对照组(生理盐水组)和EGb组,各分为5个时相点,每个时想点3只大鼠,均采用改良的Allen打击法制成中度急性脊髓损伤模型,术后EGb组给予舒血宁0.75 ml/(kg·d),对照组给予等量生理盐水.分别于术后1、3、5、7、14 d处死动物取材.[结果]显微镜下观察,阳性细胞胞浆棕黄色染色,对照组和治疗组均发现iNOS阳性细胞的表达,均在5 d达到高峰,但EGb治疗组细胞阳性率显著低于对照组(P＜0.05)[结论]EGb能够抑制iNOS的表达;抑制iNOS的表达可能是银杏叶缓解急性脊髓损伤的诸多机制之一.     

原花青素对大鼠急性脊髓损伤的保护作用及机制研究

[目的]探讨原花青素对大鼠急性脊髓损伤(spinal cord injury,SCI)的保护作用.[方法]SD大鼠随机分为假手术组(A组)、脊髓打击损伤组(B组)、原花青素治疗组(C组).A组行T8椎板切除术,不伤及脊髓.B、C组采用改良Allens撞击法制备大鼠T8急性SCI模型.C组术后立即腹腔注射原花青素100 mg/kg,A、B组术后立即腹腔注射等量的生理盐水.分别于术后不同时间点评价大鼠后肢运动功能,检测脊髓匀浆超氧化物歧化酶(superoxide dismutase,SOD)、髓过氧化物酶(myeloperoxidase,MPO)活性、丙二醛(malondialdehyde,MDA)含量改变,观察脊髓组织病理学变化.[结果]术后A组大鼠后肢运动功能恢复.术后C组大鼠后肢运动功能较B组均有所改善,72 h后肢运动功能恢复更为显著(P＜0.01).术后48 hB组脊髓组织SOD活性较A组明显降低(P＜0.01),而MDA含量较A组明显增加(P＜0.01);应用GSPE后,术后48hC组脊髓组织SOD活性较B组明显升高(P＜0.01),脊髓组织MDA水平较B明显降低(P＜0.01);SCI后脊髓组织TNF-α含量、MPO活性均随时间推移逐渐增高;各时间点C组脊髓TNF-α含量、MPO活性较B组均有统计学意义(P＜0.01);A组大鼠各检测点脊髓组织形态结构均正常;B、C两组72 h切片变化最为显著;B组可见神经组织多灶性出血、大量神经元坏死、尼氏体溶解消失、核固缩变小及炎性细胞浸润;C组可见局部出血点、细胞轻度肿胀,胞质均匀及少量炎性细胞浸润.[结论] GSPE可明显改善大鼠运动功能,抑制氧化应激、炎症反应和细胞凋亡等,对SCI有神经保护作用.     

银杏叶提取物对大鼠急性脊髓损伤后神经功能恢复的作用及其机制

目的:观察银杏叶提取物(EGb)对大鼠实验性脊髓损伤后组织结构及运动功能恢复的作用,探讨其对急性脊髓损伤的作用机制。方法:120只SD雄性大鼠,随机分为假手术组(A组)、损伤对照组(B组)、甲基强的松龙(MP)治疗组(C组)和EGb治疗组(D组),每组30只。B、C、D组用Allen′s法以50g·cm致伤大鼠T9脊髓制作损伤模型,B组为单纯脊髓损伤,不给药;C组为脊髓损伤后30min内,由腹腔注入MP30mg/kg;D组为术后至处死前每天腹腔给予EGb17.5mg/kg;A组只打开T9椎板,不打击脊髓,不给药。术后24h、3d、5d、7d、14d对大鼠进行脊髓运动功能(BBB)评分。于术后24h、3d、5d、7d、14d处死动物(n=6),取T9节段脊髓,切片苏木素-伊红(HE)染色观察脊髓大体组织结构变化,用免疫组织化学方法检测B细胞淋巴瘤/白血病基因-2(Bcl-2)和B细胞淋巴瘤/白血病基因伴随蛋白x(Bax)在脊髓前角运动神经元中的表达变化情况。结果:各时间点B、C、D组大鼠脊髓运动功能(BBB)评分均显著低于A组(P<0.01),伤后7d、14d时C、D组评分显著高于B组(P<0.05),各时间点C组与D组评分比较无统计学意义(P>0.05)。HE染色C组和D组大鼠脊髓损伤区较B组坏死程度轻、形成囊腔少,A组正常;1周后D组较C组片状出血灶少,神经细胞肿胀不明显。各时间点B、C、D组大鼠损伤脊髓前角运动神经元中Bcl-2阳性细胞数均显著高于A组(P<0.01),C、D组显著高于B组(P<0.01),7d、14d时D组显著高于C组(P<0.05);各时间点B、C、D组大鼠损伤脊髓前角运动神经元中Bax阳性细胞数均显著高于A组(P<0.01),C、D组显著低于B组(P<0.01),7d、14d时D组显著低于C组(P<0.01)。结论:EGb可能通过抑制Bax表达、提高Bcl-2表达,抑制脊髓损伤后神经元凋亡,在运动功能恢复、损伤脊髓组织保护上发挥其有益作用,1周后EGb仍能抑制脊髓损害后的继发性损伤。     

Preventive effects of Ginkgo biloba extract on ischemia-reperfusion injury in rat bladder

AIMS: The aim of this experimental study was to evaluate the effects of Ginkgo biloba (EGb 761) on ischemia-reperfusion (I-R) injury in the rat bladder. METHODS: A bladder I-R injury was induced by abdominal aorta occlusion by ischemia for 30 min, followed by 45 min reperfusion in rats. The rats were divided into four groups of 7 rats each; the control, I-R, and I-R groups were pretreated intraperitoneally with 50 or 100 mg/kg G. biloba 60 min before ischemia induction. Contractile responses to carbachol through isolated organ bath studies were recorded, histological sections were evaluated by light microscopy, and TUNEL staining was performed for the evaluation of apoptosis. RESULTS: In the I-R group, the contractile responses of the bladder strips were lower than those of the control group (p < 0.01-0.001) and were restored by pretreatment with 100 mg/kg G. biloba (p < 0.05-0.001). Decreased polymorphonuclear leukocyte infiltration was detected in the G. biloba pretreatment groups when compared to the I-R group during histological evaluation. The ratio of TUNEL-positive nuclei was 1.84% in the I-R group, whereas it was decreased in both of the G. biloba pretreatment groups (p < 0.01, p < 0.01). CONCLUSION: Our data indicated that G. biloba has a preventive effect on I-R injury in rat urinary bladder.     

银杏酮酯对大鼠坐骨神经损伤后神经生长因子基因表达的影响

目的 观察银杏酮酯（EGb50）对大鼠坐骨神经损伤后神经生长因子（NGF）mRNA表达的影响。方法 取SD大鼠78只，其中72只切断右侧坐骨神经并缝合，随机分成损伤对照组与实验组，另6只为正常对照组。实验组给予EGb50200mg／kg／d溶于1．0ml生理盐水中灌胃，损伤对照组每天给予生理盐水1．0ml灌胃，正常对照组不作任何处理。分别于术后1、3、7、14、21及28d取吻合口远段的神经、相应节段的脊神经节及脊髓，采用逆转录-多聚酶链反应技术检测所取组织中NGFmRNA的表达水平。结果 实验组坐骨神经中NGFmRNA的表达在术后7、14和21d明显高于对照组（P〈0．05）。术后7d和14d，实验组脊神经节及脊髓中NGFmRNA的表达高于对照组（P〈0．05）。结论 大鼠坐骨神经损伤后用银杏酮酯治疗，在早期可促使坐骨神经及相应节段脊神经节和脊髓组织中的NGFmRNA的表达增加。     

Protective effects of oral creatine supplementation on spinal cord injury in rats

STUDY DESIGN: To evaluate a potential protective effect of increased creatine levels in spinal cord injury (SCI) in an animal model. OBJECTIVES: Acute SCI initiates a series of cellular and molecular events in the injured tissue leading to further damage in the surrounding area. This secondary damage is partly due to ischemia and a fatal intracellular loss of energy. Phospho-creatine in conjunction with the creatine kinase isoenzyme system acts as a potent intracellular energy buffer. Oral creatine supplementation has been shown to elevate the phospho-creatine content in brain and muscle tissue, leading to neuroprotective effects and increased muscle performance. SETTING: Zurich, Switzerland. METHODS: Twenty adult rats were fed for 4 weeks with or without creatine supplemented nutrition before undergoing a moderate spinal cord contusion. RESULTS: Following an initial complete hindlimb paralysis, rats of both groups substantially recovered within 1 week. However, creatine fed animals scored 2.8 points better than the controls in the BBB open field locomotor score (11.9 and 9.1 points respectively after 1 week; P=0.035, and 13 points compared to 11.4 after 2 weeks). The histological examination 2 weeks after SCI revealed that in all rats a cavity had developed which was comparable in size between the groups. In creatine fed rats, however, a significantly smaller amount of scar tissue surrounding the cavity was found. CONCLUSIONS: Thus creatine treatment seems to reduce the spread of secondary injury. Our results favour a pretreatment of patients with creatine for neuroprotection in cases of elective intramedullary spinal surgery. Further studies are needed to evaluate the benefit of immediate creatine administration in case of acute spinal cord or brain injury.     

银杏叶提取物对周围神经损伤后运动神经元的保护作用

目的　研究银杏叶提取物在大鼠坐骨神经损伤后对运动神经元的保护作用。方法　SD大鼠 3 6只 ,按手术先后随机平分为银杏叶提取物 (EGb 761)组和生理盐水 (SAL)组。大鼠均制成坐骨神经部分切除后结扎断端的模型 ,术后每天经腹腔分别注射EGb 761(10 0mg/kg-1·d-1)和同体积的生理盐水直到取材。术后 2、4、6周取材 ,大鼠处死后取L4～ 6节段脊髓 ,经酶组化染色后观察乙酰胆碱脂酶 (AChE)及酸性磷酸酶 (ACP)的活性变化 ;冰冻切片硫槿染色后对前角大型运动神经元计数 ;电镜观察脊髓前角运动神经元超微结构的变化。结果　与对照组相比 ,银杏叶提取物组的乙酰胆碱脂酶、酸性磷酸酶活性、损伤侧前角运动神经元数目及前角运动神经元超微结构 ,均有明显的改善。结论　银杏叶提取物对周围神经损伤后的脊髓前角运动神经元损害有保护作用     

神经生长因子对大鼠脊髓损伤后一氧化氮合成酶含量的影响

探讨神经生长因子（ＮＧＦ）对脊髓损伤保护作用的机制。方法采用Ａｌｉｅｎ’ｓ法以２５ｇｃｍ致伤大鼠Ｔ８脊髓,经蛛网膜下腔导管分别于术后即刻、３０分钟、１、２、３、４、８、１２、２４小时各注入ＮＧＦ溶液,并与生理盐水组和正常对照组作对照。采用放射强度测定法测定一氧化氮合成酶（ＮＯＳ）含量。结果与正常组相比较,ＮＯＳ含量在伤后１０分钟、１、２、４、８小时均显著升高（Ｐ＜０．０１）,ＮＧＦ治疗组与生理盐水组相比较,在伤后１０分钟、１、２、４、８小时ＮＯＳ活性明显下降（Ｐ＜０．０１）。结论ＮＧＦ通过抑制脊髓损伤后ＮＯＳ的升高效应,抑制了一氧化氮（ＮＯ）的神经毒性作用,从而保护了神经组织。     

锂剂抑制脊髓损伤后大鼠细胞凋亡的机制研究

目的 :研究锂剂是否通过抑制脊髓损伤(spinal cord injury,SCI)后大鼠神经细胞的凋亡产生神经保护作用。方法:将42只SD雄性大鼠,体重为200~250 g,按随机数字法分成3组:空白对照组(6只)不做手术;生理盐水(NS)组(18只)经腹腔注射NS(40 mg/kg);氯化锂(Licl)组(18只)经腹腔注射Licl(40 mg/kg)。按照Allen法对大鼠建模后,Licl组于脊髓损伤术后15 min内开始腹腔注射Licl溶液(40 mg·kg~(-1)·d~(-1))2周,NS组在同时间内注入等量的NS作为对照。分别于术后3、7、14 d进行BBB评分,利用免疫组化染色观察Bcl-2和Bax的表达,并采用TUNEL染色观察神经细胞凋亡。结果:BBB评分:空白对照组大鼠为21±0,Licl组与NS组比较,术后7、14 d时Licl组大于NS组(P0.05)。Bcl-2蛋白表达:空白对照组大鼠为0.081±0.003,术后7、14 d两个时间点Bcl-2蛋白表达Licl组分别为0.151±0.003和0.163±0.003,NS组为0.143±0.003和0.154±0.002,Licl组能明显升高其表达(P0.05)。Bax蛋白的表达:空白对照组大鼠为0.071±0.003,术后7、14 d两个时间点Bax蛋白的表达Licl组分别为0.121±0.002和0.106±0.002,NS组为0.126±0.001和0.120±0.002,Licl组可以明显降低其表达(P0.05)。神经细胞凋亡:TUNEL染色显示,空白对照组阳性细胞较少,凋亡指数(AI)为1.98±0.19,术后7、14 d两个时间Licl组分别为13.12±0.69和4.29±1.00,NS组为18.26±0.87和5.48±0.70,Licl组能显著抑制细胞凋亡(P0.05)。结论 :锂剂能够促进SCI后大鼠的神经元细胞内Bcl-2蛋白的表达,抑制神经元内Bax蛋白的表达,从而起到了抑制神经细胞凋亡的作用,这可能是锂剂促进大鼠运动功能恢复的机制之一。     

Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats

OBJECTIVE: To explore the molecular mechanism of the protective effect of nerve growth factor (NGF) on injured spinal cord. METHODS: The posterior T(8) (the 8th thoracic segment) spinal cords of 60 Wistar rats were injured by impacts caused by objects (weighing 10 g) falling from a height of 2.5 cm with Allen's way. Solution with nerve growth factors (NGF) was given to 30 rats (the NGF group) through a microtubule inserted into the subarachnoid cavity immediately, and at 2, 4, 8, 12 and 24 hours after spinal cord injury (SCI) respectively. Normal saline (NS) with same volume was given to the other 30 rats (the NS group) with the same method. And 5 normal rats were taken as the normal controls. The expression of bcl-2 and bax proteins in spinal cord was detected with immunohistochemistry. The apoptotic neurons in spinal cord were measured with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling of DNA fragments (TUNEL) staining. RESULTS: The positive expression of bcl-2 protein was strong in the normal controls, but decreased in the NS group, and increased significantly in the NGF group as compared with that of the NS group (P<0.01). The positive expression of bax protein was also strong in the normal controls, but increased in the NS group, and decreased significantly in the NGF group as compared with that of the NS group (P<0.01). Apoptotic neurons were found in the NS group, and they decreased significantly in the NGF group as compared with that of the NS group (P<0.01). CONCLUSIONS: NGF can protect the injured nerve tissues through stimulating the expression of bcl-2 protein, inhibiting the expression of bax protein and inhibiting the neuronal apoptosis after SCI.