安多霖对微波辐射致大鼠脑损伤的预防作用研究

目的 探讨安多霖对微波辐射致大鼠脑损伤的预防作用.方法 140只二级雄性Wiser大鼠随机分为5组:健康对照组、辐射对照组、低浓度(0.75 g·kg～·d-1)预防组、中浓度(1.5 g·kg～·d-1)预防组及高浓度(3 g·kg～·d-1)预防组.预防组每日1次灌胃给予安多霖溶液,连续给药工2周.给药结束后采用30 mW/cm.微波辐射大鼠15 min.于处理后6 h、7 d和14 d,采用Morris水迷宫检测大鼠学习和记忆能力,高效液相色谱检测海马氨基酸类神经递质含量,光镜和电镜观察海马组织学和超微结构变化.结果 微波辐射后7 d内,大鼠学习和记忆能力下降(F=0.000～0.043,P<0.05);微波辐射后6 h,4种氨基酸类神经递质含量均降低,其中谷氨酸、甘氨酸及γ-氨基丁酸降低明显(F=0.000～0.007,P<0.01);微波辐射后6 h、7 d,海马组织水肿,神经元变性;神经元线粒体肿胀、空化,内质网扩张,突触间隙模糊,血管周间隙增宽.低浓度预防组上述变化与辐射对照组相似.中浓度和高浓度预防组微波辐射后7 d内,大鼠学习和记忆能力损伤不明显,两者与辐射对照组相比,差异有统计学意义(F=0.015～0.028,P<0.05);微波辐射后6 h,4种氮基酸类神经递质含量均无明显下降,其中谷氨酸含量接近正常,两者与辐射对照组比,差异有统计学意义(F=0.000-0.042,P<0.05);微波辐射后6 h、7 d,海马组织无明显损伤.结论 30 mW/cm.微波辐射可引起大鼠学习和记忆能力下降、海马氨基酸类神经递质代谢紊乱及海马组织学和超微结构损伤;1.5和3 g·kg-1·d-1安多霖对微波辐射致大鼠脑损伤有预防作用.1.5 g·kg-1·d-1安多霖为预防微波辐射致大鼠脑损伤的有效剂量.

Abstract：

Objective To study the prevention effects of AduoLa Fuzhenglin(ADL)Oll the brain injury induced by microwave radiation in rats.Methods A total of 140 male Wismr rats were divided randomly into 5 groups,including control group,microwave exposed group,low dosage(0.75 g·kg-1·d-1)group.middle dosage(1.5 g·kg-1·d-1)group and high dosage(3 g·kg-1·d-1)group.Rats in three ADL groups were lavaged with ADL per day for 2 weeks before radiation.After administration,rats were exposed to microwave at 30 mW/cm2 for 15 min.The abilities of learning and memory were detected by Morris water maze,and the contents of amino acids neurotransmitter of hippocampus were detected by HPLC, then the histology and uhrastrncture of hippocampus were observed with light and electron microscope at 6 h,7 and 14 d after exposure.Results The abilities of learning and memory were declined(F=0.000-0.043,P<0.05)from 6 h to 7 d after exposure,and the contents of four kinds of amino acid neurotransmitter in hippocampus were decreased,of which GLU,GLY and GABA were decreased significantly(F=0.000-0.007,P<0.01)at 6h after exposure,then tissue edema,neuronal degeneration,neuron mitoehondria swelling and cavitation,endocytoplasmie rotieulum broaden,synaptic cleft blurred,and perivascular space widen were found in the hippocampus at 6 h and 7 d after exposure.The changes in low dosage group were similar to those of the radiation group.However,in middle and high dosage groups,the abilities of learning and memory were normal to some extent with the significant differences compared to the radiation group from 6 h to 7 d after exposure(F=0.015-0.028.P<0.05).The contents of four kinds of amino acid neurotransmitter were not decreased,especially GLU contents close tO normal level.There were significant differences between middle and high dosage groups and radiation group at 6 h after exposure(F=0.000-0.042,P<0.05).Moreover,no obvious injury in the hippocampus was observed in middle and high dosage groups at 6 h and 7 d after exposure.Conclusions Exposure to 30 mW/cm2 microwave radiation could decrease the abilities of learning and memory,induce amino acid neurotransmitter turbulence,and injure the histology and uhrastructure of hippocampus.ADL at the dosages of 1.5 and 3 g·kg-1·d-1 would have preventive effects on the injury induced by microwave exposure.The concentration of 1.5 g·kg-1 ·d-1 of ADL might be the effective dosage to prevent the brain damage after microwave exposure.     

安多霖对微波辐射致大鼠脑损伤的预防作用研究

Objective To study the prevention effects of AduoLa Fuzhenglin(ADL)Oll the brain injury induced by microwave radiation in rats.Methods A total of 140 male Wismr rats were divided randomly into 5 groups,including control group,microwave exposed group,low dosage(0.75 g·kg-1·d-1)group.middle dosage(1.5 g·kg-1·d-1)group and high dosage(3 g·kg-1·d-1)group.Rats in three ADL groups were lavaged with ADL per day for 2 weeks before radiation.After administration,rats were exposed to microwave at 30 mW/cm2 for 15 min.The abilities of learning and memory were detected by Morris water maze,and the contents of amino acids neurotransmitter of hippocampus were detected by HPLC, then the histology and uhrastrncture of hippocampus were observed with light and electron microscope at 6 h,7 and 14 d after exposure.Results The abilities of learning and memory were declined(F=0.000-0.043,P<0.05)from 6 h to 7 d after exposure,and the contents of four kinds of amino acid neurotransmitter in hippocampus were decreased,of which GLU,GLY and GABA were decreased significantly(F=0.000-0.007,P<0.01)at 6h after exposure,then tissue edema,neuronal degeneration,neuron mitoehondria swelling and cavitation,endocytoplasmie rotieulum broaden,synaptic cleft blurred,and perivascular space widen were found in the hippocampus at 6 h and 7 d after exposure.The changes in low dosage group were similar to those of the radiation group.However,in middle and high dosage groups,the abilities of learning and memory were normal to some extent with the significant differences compared to the radiation group from 6 h to 7 d after exposure(F=0.015-0.028.P<0.05).The contents of four kinds of amino acid neurotransmitter were not decreased,especially GLU contents close tO normal level.There were significant differences between middle and high dosage groups and radiation group at 6 h after exposure(F=0.000-0.042,P<0.05).Moreover,no obvious injury in the hippocampus was observed in middle and high dosage groups at 6 h and 7 d after exposure.Conclusions Exposure to 30 mW/cm2 microwave radiation could decrease the abilities of learning and memory,induce amino acid neurotransmitter turbulence,and injure the histology and uhrastructure of hippocampus.ADL at the dosages of 1.5 and 3 g·kg-1·d-1 would have preventive effects on the injury induced by microwave exposure.The concentration of 1.5 g·kg-1 ·d-1 of ADL might be the effective dosage to prevent the brain damage after microwave exposure.     

安多霖对微波辐射致大鼠海马细胞色素C氧化酶变化的影响

目的探讨中药复方制剂（安多霖）对微波辐射后大鼠海马线粒体呼吸链细胞色素C氧化酶（cytochromec oxidase,COX）变化的影响。方法 100只Wistar雄性大鼠随机分为3个对照组,即正常对照组、辐射预防对照组、辐射治疗对照组和2个安多霖组,即3 g/（kg.d）安多霖预防组及3 g/（kg.d）安多霖治疗组,每组20只。安多霖预防组大鼠于给药后第15天进行微波辐射;安多霖治疗组大鼠于辐射后当天开始连续给药14 d,均1次/d。采用30 mW/cm2微波辐射15 min,于辐射后6 h和14 d活杀动物取海马,通过比色法检测大鼠海马COX活性的变化;采用实时定量PCR和Western印迹检测大鼠海马COXⅠ、ⅣmRNA以及COXⅠ蛋白表达变化。结果辐射预防和治疗两对照组于停药后6 h COX活性、COXⅠ、ⅣmRNA,COXⅠ蛋白均降低（P〈0.05或P〈0.01）;安多霖预防组较辐射预防对照组COX活性及基因表达有不同程度提高,与正常对照组无明显差异;安多霖治疗组与辐射治疗对照组相比明显提高（P〈0.05）,且基本恢复正常。结论给予3 g/（kg.d）安多霖对微波辐射致大鼠海马线粒体呼吸链COX表达降低有较明显改善作用,其治疗效果更为显著。     

安多霖对高功率微波辐射大鼠生精细胞凋亡的影响及机制研究

目的 探讨安多霖对微波辐射的防护作用及作用机制。方法 选用SPF级雄性SD大鼠,随机分为3个给药组,剂量分别为3、6、9 g/kg,另设辐射模型组和健康对照组,每组20~21只。给药组大鼠连续灌胃安多霖20 d ,停药后,给药组和辐射模型组动物行一次平均功率密度为100 mW/cm²高功率微波全身辐照10min,健康对照组不辐照。动物分别于辐照后24、48 h和5 d 取睾丸组织,制作睾丸石蜡切片,采用原位末端标记术(TUNEL)检测睾丸生精细胞凋亡,免疫组化法检测细胞凋亡相关蛋白Bax和Bcl-2。结果 微波辐射后24、48 h和5 d,与健康对照组相比,辐射组睾丸生精细胞的凋亡数明显升高(t=-41.89、-11.29、-62.24,P<0.05),Bcl-2/Bax比值明显降低(t=8.49、4.36、4.47,P<0.05);而与辐射组相比,低、中和高剂量给药组的凋亡细胞数显著降低(F=5.25、9.79、15.35, P<0.05), Bcl-2/Bax比值明显升高(F=20.17、11.75、11.98, P<0.05)。结论 高功率微波辐射可诱导大鼠生精细胞凋亡增加,安多霖对细胞凋亡有明显抑制作用。安多霖抑制大鼠睾丸生精细胞凋亡的机制可能与其能够上调Bcl-2及下调Bax蛋白的表达,改变了Bcl-2/Bax的比值有关。     

安多霖对微波辐射致大鼠心肌细胞半胱天冬酶-3表达的影响

目的探讨抗辐射中药复方安多霖对微波辐射后大鼠心肌细胞半胱天冬酶（caspase）-3表达的改变及其意义。方法将140只二级雄性Wistar大鼠随机分为正常对照组、辐射对照组、安多霖0.75 g/（kg.d）、1.5 g/（kg.d）及3 g/（kg.d）预防组。预防组每日1次灌胃给予安多霖溶液,连续给药2周。给药结束后即刻30 mW/cm2微波辐射大鼠1次,辐射时间为15 min。于停药后7 d和14 d,采用Western印迹法、免疫组织化学和图像分析技术,研究大鼠心脏细胞caspase-3表达的变化规律。结果停药后7和14 d,辐射对照组大鼠心肌细胞caspase-3主要位于胞浆,其蛋白表达显著升高（P〈0.01）;0.75 g/（kg.d）安多霖预防组大鼠心肌细胞caspase-3表达与辐射对照组相似;1.5 g/（kg.d）和3 g/（kg.d）安多霖预防组大鼠心肌细胞caspase-3表达比辐射对照组显著下降（P〈0.01）。结论 30 mW/cm2微波辐射可引起大鼠心肌细胞caspase-3表达增强;给予安多霖1.5和3 g/（kg.d）对微波辐射致大鼠心肌caspase-3表达升高有降低作用;安多霖对微波辐射引起心脏损伤的预防作用可通过下调caspase-3表达来实现。     

安多霖对高功率微波辐射大鼠生精细胞凋亡的影响及机制研究

Objective To investigate the protection function of Anduolin (ADL) against exposure to high power microwave,and to probe the mechanism involved.Methods The SPF-class nude rats were randomly divided into ADL groups (Dose of 3,6 and 9 g/kg body weight),model group and control group.Rats in ADL groups were continuously ingested with ADL for 20 d.The rats in ADL groups and model group were exposed to high power microwave at average power density of 100 mW/cm2 for 10 min.Their testes were excised at 24 h,48 h and 5 d after exposure to microwave.Apoptosis of spormatogenic cells and the expression of Bax and Bcl-2 were detected with in situ end-labeling method and immuno-histochemistry method,respectively.Results At 24 h,48 h and 5 d after exposure to high power microwave,compared with control group,the counts of apoptotic spermatagenic cells in exposed model group were increased significantly (t=-41.89,-11.29 and -62.24,P＜0.05),while the ratio of Bcl-2/Bax in exposed group was decreased significantly( t=8.49,4.36 and 4.47,P＜0.05).At the same time,compared with the exposed group,the counts of apoptotie spormatogenic cells in 3,6,and 9 g/kg ADL groups were reduced significandy( F=5.25,9.79 and 15.35,P＜0.05),while the ratio of Bcl-2/Bax was enhanced significandy( F=20.17,11.75 and 11.98,P＜0.05).Conclusions The high power microwave could induce the apoptosis of spermatogenic cells.ADL protect the spermatogenic cells via the ratio Bel-2/Bax increasing.     

安多霖对微波辐射致大鼠胸腺和脾脏组织学及超微结构损伤的预防作用研究

目的观察安多霖对微波辐射致大鼠胸腺和脾脏组织学及超微结构损伤的预防作用。方法 Wistar雄性大鼠280只,随机分为短期（14 d）及长期（28 d）安多霖预防组,每组140只。每组又随机分为空白对照组、辐射组及0.75、1.5、3 g/（kg.d）安多霖预防组。辐射组及预防组动物连续灌胃给药14 d（每天1次）后进行30 mW/cm2微波辐射15 min,于停药（辐射）后6 h、7 d及14 d将动物分批活杀,采用光镜及电镜观察胸腺和脾脏的组织学及超微结构改变。结果短期安多霖预防组：停药后6 h及7 d,辐射组及0.75 g/（kg.d）安多霖预防组大鼠脾脏组织学及超微结构明显损伤,胸腺无明显改变;1.5及3 g/（kg.d）安多霖预防组：辐射后6 h及7 d,脾脏改变较辐射组明显减轻,停药后14 d各组病变基本恢复;长期预防组改变与短期预防组规律相同。结论预防性给予1.5 g/（kg.d）安多霖可对30 mW/cm2微波辐射引起的大鼠免疫器官结构损伤有明显的改善作用;给药28 d与给药14 d效果无明显差异。     

电磁脉冲致大鼠睾丸组织急性损伤的超微结构研究

目的 :通过观察电磁脉冲 (EMP)辐照大鼠后其睾丸组织学及超微结构的急性改变 ,初步探讨EMP致睾丸损伤的特点。方法 :雄性二级Wistar大鼠 2 4只 ,随机分为 6组 ,每组 4只。其中 1组为对照组 ,其余 5组为辐照组。辐照组在高场强电磁脉冲模拟源下 ,以场强为 6× 10 4 V·m-1,脉冲上升时间为 2 0ns,脉宽为 30 μs的条件下 ,在 2min内辐照大鼠 5次 ,对照组不做任何处理 ,辐照后于 1、6、12、2 4和 48h活杀动物 ,电镜制片 ,PHILIPS -CM12 0电镜下观察、拍片。结果 :被辐射组大鼠睾丸精原细胞和间质细胞超微结构 6h后变化明显 ,线粒体水肿、空化、髓样体形成 ;内质网扩张 ;糖原颗粒减少。睾丸间质细胞的内分泌颗粒排空明显。结论 :EMP辐照后早期即可引起大鼠睾丸精原细胞及间质细胞损伤 ,细胞膜系统的损伤及应激反应可能参与了其超微结构损伤过程 ,睾丸间质细胞可能为电磁脉冲损伤的敏感细胞之一     

电磁脉冲辐照对培养大鼠垂体细胞上清中LDH、AST、CHE、K+ 和Na+ 的影响

对Wistar大鼠垂体细胞在6孔板中进行原代培养,在培养第4天时,用高场强EMP模拟源(场强为6×104 V/m,脉冲上升时间为20ns,脉宽为30μs),2min内辐照5次.并于辐照后0(即刻)、1、6、12和24h应用中生公司生化检测试剂盒测定培养上清中LDH、AST、CHE、K+、Na+浓度,探讨电磁脉冲对垂体细胞损伤的机制.结果表明,电磁脉冲辐照后即刻就可引起培养上清LDH和CHE明显升高;辐照后1和6h培养上清中LDH、AST、CHE、和K+明显升高;辐照后12h培养上清中LDH、AST和K+明显升高;辐照后24h所有上述指标基本恢复.结果提示,电磁脉冲辐照后可引起大鼠垂体细胞膜的损伤.     

高场强电磁脉冲辐射对小鼠肝细胞DNA含量和倍体影响的定量学研究

目的　动态观察高场强电磁脉冲辐射 (EMP)对小鼠肝细胞核DNA含量及倍体的影响 ,探讨电磁辐射的生物学效应。方法　应用高场强EMP发射源对二级昆明小鼠进行全身辐射 ,场强分别选用 8× 10 3、2× 10 4 和 6× 10 4 V m ,发射源相关技术参数 :脉冲上升时间 2 0ns,脉宽 30 μs ,2min内发射 5个单脉冲 ;采用Feulgen染色动态观察小鼠肝细胞核内DNA含量的变化 ,观察时间 1年 ,共设 10个时相点 (n =6 ) ,并用德国IBSA显微数字图像分析系统作DNA含量定量分析和倍体分型。结果　小鼠经高场强EMP辐射后 3个月内 ,肝细胞核DNA含量与正常对照组差异无显著性 ,以二倍体细胞 (2C)为主 ,四、六倍体 (4C ,6C)较少 ,八倍体 (8C)偶见 ;辐射后 6个月 ,8× 10 3V m辐射组比对照组DNA含量高 (P <0 0 5 ) ,2C数量减少 ,4C和 6C增加 ;至辐射后 9个月和 12个月 ,各辐射组肝细胞核DNA含量比其他各时相点辐射组及同一时相点对照组显著增高 (P <0 0 1) ,并且以 4C为主 ,6C和 8C增加 ,而 2C明显减少。结论　高场强EMP对小鼠肝DNA含量及倍体有影响 ,且表现为远后效应 ,推测电磁辐射对肝的生物学效应中肝细胞核酸可能是一个重要的靶点 ,这将为进一步研究其损伤效应及其作用机制提供实验性依据。此外 ,本研究结果提示要注重电磁辐射远     

次声下大鼠肝细胞损伤作用的超微结构变化

目的：探讨次声下大鼠肝细胞损伤特点及意义。方法：将雄性SD大鼠36只随机分为对照组和1d、7d、14d、21d和28d共6组，实验组在16Hz次声130db环境下每日暴露1次，每次2h；取其肝汇管区和右叶边缘区两个部位肝组织用戊二醛和锇酸固定，透射电镜下观察肝超微结构变化。结果：不同环境和天数次声作用后肝损伤以脂代谢紊乱和变性坏死为主，可见肝细胞脂代谢紊乱和肝细胞内的各种结构早期随作用次数增多其损伤逐渐加重，28d组其损伤程度有所恢复。结论：次声下可以对肝细胞及组织造成不同程度损伤，28d后肝组织对次声损伤作用存在着一定适应现象。     

高功率脉冲微波辐照对大鼠血清激素水平影响的研究

目的：通过对高功率脉冲微波（HPPMW）辐照后Wistar大鼠血清中睾酮（Testo)、雌二醇（E2）、促甲状腺激素（TSH）、游离甲状腺素T4（FT4）、皮质醇（Cort)、醛固酮（Ald)及生长激素（HGH）的动态观察,以探讨HPPMW对内分泌系统的影响。用高功率脉冲微波源,以功率密度为3050W／cm^2脉冲微波（频率为5．4GHz,脉宽为26ns)辐照辐照组动物。于辐照后1h,6h,24h,7d,14d及28d分别采血,用放射免疫法在FT630放免疫定仪上进行统一测定。所有数据经SPSS8．0统计处理。结果：大鼠被辐照后,其血清E2在早期变化不明显,但在14d时明显升高（P＜0．01）;Testo辐照后1h和14d明显下降（P＜0．05）;TSH于辐照后逐渐升高,14d到28d时明显增高（P＜0．05）;FT4辐照后1h明显升高（P＜0．05）;TSH于辐照后逐渐升高,14d到28d时明显增高（P＜0．05）;FT4辐照后1h明显升高（P＜0．05）后逐渐降低,在28d下降到最低点（P＜0．01）;Cort辐照后1h即升高,14d达到峰值（P＜0．05）;Ald于照后6h-14d略低于对照组,28d恢复;HGH辐照后明显低于照前水平,在28d下降到最低点（P＜0．05）。结论LHPPMW可引起大鼠血清激素水平的紊乱。既有早期影响,也表现为一定的持续效应。提示HPPMW可能直接引起大鼠内分泌系统的损伤。     

WT对辐射致DNA损伤修复的影响

目的 研究磷脂酰肌醇３－激酶的特异性抑制剂Ｗｏｒｔｍａｎｎｉｎ（ＷＴ）对小鼠胸腺细胞ＤＮＡ辐射损伤的修复的影响,以探索ＷＴ放增敏作用机制。方法 以５０μｍｏｌ／Ｌ ＷＴ作用小鼠胸腺细胞,以不同剂量γ－射线照射,照射后不同时间制取细胞ＤＮＡ糖浆胶电泳方法检测ＤＮＡ双链断裂（ｄｓｂ）。结果 ＷＴＯ单独对受照射细胞ｄｓｂ产额无明显影响,抑制照射后ｄｓｂ。结论 ＷＴ的放射增敏剂作用与其抑制照射后ｄｓｂ修复     

三氧化二砷对白血病细胞DNA损伤及凋亡相关基因表达的影响

目的：研究三氧化二砷（As2O3)对HL－60，K562和NB4细胞DNA的损伤及凋亡相关基因的调控。方法：用荧光显微技术，单细胞彗星电泳观察As2O3对HL－60，K562及NB4细胞DNA的损伤，用流式细胞术测定As2O3对HL－60，K562及NB4细胞凋亡相关基因Bcl-2和p53的表达，结果：As2O3诱导HL－60，K562和NB4细胞的凋亡时造成了DNA损伤；显著下调三种细胞内Bcl-2蛋白的表达，且Bcl-2下调程度与凋亡有密切关系，上调了p53蛋白的表达。结论：As2O3诱导细胞凋亡时发生了DNA的损伤，诱导凋亡主要是通过下调Bcl-2和上调p53来实现。     

低剂量辐射对环磷酰胺所致DNA损伤的影响

目的研究低剂量γ射线预照射对大剂量环磷酰胺化疗所致外周血淋巴细胞DNA损伤及遗传物质损伤的影响。方法昆明种雄性小鼠随机分为空白对照组、荷瘤对照组（假照组）、荷瘤低剂量照射组（LDR组）、荷瘤环磷酰胺化疗组（CTX组）和荷瘤低剂量照射联合化疗组（LDR＋CTX组）。常规饲养1周后，于左腹股沟皮下各接种S180肉瘤细胞（空白对照组除外），接种后第8和11天对LDR组和LDR＋CTX组小鼠给予75mGy-γ射线全身照射，照射后30h分别给予CTX组和LDR＋CTX组小鼠腹腔注射环磷酰胺3．0mg；第13天处死所有小鼠，分别取血，采用单细胞凝胶电泳法检测外周血淋巴细胞DNA损伤；采用骨髓嗜多染红细胞微核率（MNF）检测遗传物质损伤。结果①环磷酰胺化疗后DNA损伤程度较空白对照及荷瘤对照组均显著增加；环磷酰胺化疗前给予75mGy-γ射线照射，则可显著降低大剂量环磷酰胺化疗所致的DNA损伤。②大剂量环磷酰胺化疗后小鼠骨髓嗜多染红细胞微核率较空白对照组及单纯荷瘤组有显著增加（P〈0．01）；环磷酰胺化疗前给予75mGy-γ射线照射则可降低环磷酰胺所致微核率的增加，但差异无统计学意义（P〉0．05）。结论①大剂量环磷酰胺化疗可引起外周血淋巴细胞DNA损伤；化疗前给予75mGy-γ射线照射对DNA损伤可能产生一定的保护作用。②环磷酰胺有强大的致突变作用，可导致骨髓嗜多染红细胞微核率显著增加，75mGy-γ射线预照射对大剂量环磷酰胺化疗的遗传学毒性未表现出明显的保护作用。     

强噪声暴露对大鼠急慢性胃粘膜损伤的影响

急慢性胃粘膜损伤是常见的一种病症,对其基础与临床研究已做了大量工作.长期在噪声环境下工作和生活的人群(包括部队官兵),其胃肠疾患发生率显著增高.如何防治噪声性胃肠损伤及探讨其机理已是重要课题,为此,我们制作了大鼠急性胃粘膜损伤和大鼠胃溃疡模型并进行强噪声刺激实验,旨在观察噪声与胃粘膜损伤之间的关系,现报告如下.     

大鼠脊髓损伤后神经生长因子对内皮素含量的影响

目的　探讨神经生长因子对大鼠脊髓损伤保护作用的机理。方法　采用改良Allen’s法 10g× 2 5cm致伤大鼠第 12胸椎脊髓 ,经蛛网膜下腔导管分别于术后即刻、1、4、8、2 4、72h各注入神经生长因子溶液 ,并与生理盐水组和正常对照组作对照。采用放射免疫方法测定内皮素含量。结果　与正常组相比较内皮素含量在伤后均显著升高 (P <0 0 1) ,神经生长因子治疗组与生理盐水组相比较 ,在伤后 4、8、2 4、72h ,内皮素含量明显下降 (P <0 0 1)。结论　神经生长因子通过抑制脊髓损伤后继发作用 ,抑制了内皮素导致的恶性循环 ,从而保护了神经组织     

DNA的损伤修复能力对GPA基因突变频率的影响及其检测方法

血型糖蛋白A（GPA）基因突变频率在作为生物剂量计及癌的风险预测方面最大的缺陷在于个体差异大。DNA损伤及修复能力是影响GPA基因突变频率个体差异的决定因素之一。随着现代分子生物学实验技术的发展,检测DNA损伤及修复能力的方法不断出现,例如中性膜洗脱法、单细胞凝胶电泳、梯度电压凝胶电泳等,使得应用DNA损伤及修复能力对GPA基因突变频率的个体差异进行修正成为可能。