背根神经节内注射药物对髓核致炎作用的影响

目的探讨背根神经节（DRG）内注射药物对髓核所致炎性神经痛的作用。方法大鼠自体髓核移植至单侧L5，L6神经节周围，观察大鼠机械刺激，热刺激回缩阈值变化率及背根神经节形态学改变。给予相应致炎神经节内药物干预，观察其对大鼠行为学及相应神经节形态学改变的影响。结果自体髓核移植可以导致明显的机械刺激痛觉过敏及神经节的炎性病理改变，背根神经节内注射地塞米松，可以显著改善髓核所致的机械刺激痛觉过敏（P〈0．05）及炎性反应的程度。结论背根神经节内注射地塞米松有助于改善髓核组织引起的炎性神经痛。     

Walker256乳腺癌细胞构建大鼠胫骨骨癌痛模型

目的：探讨以Walker256大鼠乳腺癌腹水瘤细胞制备大鼠胫骨骨癌痛模型，为骨癌痛机制和治疗研究提供有用的工具。方法：以Walker256乳腺癌细胞接种幼年雌性SD鼠腹腔制备腹水瘤细胞，将15μl腹水瘤细胞注入雌性成年SD鼠左侧胫骨骨髓腔制备骨癌痛模型；以注射加热灭活瘤细胞的SD鼠为假手术对照鼠，以正常鼠为正常对照鼠。造模后1-4周观察模型鼠自由行走痛评分、辐射热痛觉阈值[缩爪反应潜伏期（paw withdrawal latency，PWL）]和机械刺激诱发痛觉阈值[缩爪反应阈值（paw withdrawal threshold，PWT）]改变，并对痛觉行为改变明显的模型鼠进行影像学检测。结果：本方法制备模型的成瘤率为67．3％。模型鼠在造模后15d自由行走痛评分显著高于正常鼠和假手术鼠（P〈0．01）；模型鼠的模型后肢对热刺激痛觉阈值和对机械刺激诱发痛觉阈值分别在造模后21d和18d明显低于正常鼠和假手术鼠（P〈0．01），同时也明显低于模型肢对侧后肢（P〈0．05）。影像学结果显示，痛行为改变明显的模型鼠模型后肢胫骨骨质结构遭到明显破坏。结论：采用Walker256乳腺癌腹水瘤细胞可成功制备与人类骨癌痛体症相似的大鼠胫骨骨癌痛模型。     

大鼠骨癌痛模型的建立及组织学研究

目的建立一个有用的癌痛动物模型.方法将MRMT-1大鼠乳腺癌细胞接种到SD大鼠胫骨上段骨髓腔内,造成骨癌痛动物模型.用von Frey细丝刺激足底和后肢负重测量仪分别测量机械性痛觉超敏和痛觉过敏,放射学方法评估骨破坏,同时,组织切片镜下观察肿瘤和骨结构的破坏情况.结果造模动物在14天左右开始出现机械性痛觉超敏和痛觉过敏,胫骨X线摄片显示明显的骨破坏,组织学研究显示骨髓腔内肿瘤生长,向外侵蚀破坏骨皮质,同时伴有新生的编织骨形成.结论从疼痛行为学、放射学、组织学多方面研究的结果,表明大鼠骨癌痛模型已复制成功.该癌痛模型的建立,将为我国癌痛新药的评价,尤其是研究治疗癌痛中药的疗效及作用机制提供一个有用的工具.     

大鼠乳腺癌骨转移模型中PI3K/Akt信号通路参与诱导疼痛

目的 探讨骨癌痛大鼠模型中PI3K/Akt信号通路参与痛觉过敏的产生和维持及其脊髓机制.方法 Wistar大鼠,体重在180~200 g,将大鼠随机分为3组:癌痛模型组(A组)、假手术组(B组)、正常组(C组),A组大鼠左侧胫骨髓腔内单次注入Walker256乳腺癌细胞建立大鼠胫骨癌痛模型,B组大鼠左侧胫骨注入等量生理盐水,C组做不给药处理.A组造模后第7天,评估筛选成模的大鼠,随机分为3组:癌痛组(A1组)、癌痛+NS组(A2组)、癌痛+抑制剂组(A3组).正常对照组(C组)随机分为2组:空白对照组(C1组)、空白+抑制剂组(C2).A3组和C2组分别在第13、14、21天鞘内注射Akt抑制剂GSK690693,A2组在第13、14、21天鞘内注射等量生理盐水,A1组、B组、C1组均不给药处理.在第0、7、14、21天,分别检测大鼠机械性缩足阈值(mechanical withdrawal threshold,MWT)和热缩腿潜伏期(thermal withdrawal latency,MWT).第21天行为学测试后处死大鼠,取大鼠脊髓L4~L6区段,用免疫组化及Western blot检测大鼠脊髓的磷酸化Akt(p-Akt)水平.结果 实验观察到大鼠的MWT和TWL均显著降低,第7天及14天A1组、A2组、A3组及B组分别与C1组比较,P<0.05,第21天A3组与A1组、A2组分别比较,P<0.05.与C1组比较,骨癌痛模型组大鼠脊髓背角p-Akt表达增强,鞘内注射Akt抑制剂可降低脊髓背角p-Akt的表达.结论 PI3K/Akt信号通路参与了骨癌痛的中枢敏化,在大鼠骨癌痛发生发展过程中起着重要作用.     

小鼠跟骨癌性疼痛模型的制备

[目的]复制一个骨癌性疼痛动物模型。[方法]将NCTC2472纤维肉瘤细胞接种到C3H／He小鼠跟骨骨髓腔内,建立骨癌性疼痛动物模型。用von Frey细丝刺激小鼠足底测量机械性痛觉超敏,冷板法测量冷痛觉过敏,组织切片镜下观察肿瘤生长和骨结构的破坏情况。[结果]造模小鼠在3天左右开始出现机械性痛觉超敏，第7天出现冷痛觉过敏,组织学研究显示骨髓腔内肿瘤生长,向外侵蚀破坏骨皮质,10天左右跟骨骨皮质明显破坏。[结论]行为学、组织学研究表明，NCTC2472纤维肉瘤细胞接种到小鼠跟骨骨髓腔的癌性疼痛模型复制成功。     

胫骨内接种建立乳腺癌骨转移大鼠模型的特点

目的研究胫骨内接种MRMT-1细胞制作的乳腺癌骨转移大鼠模型在行为学、影像学、核医学、病理学和分子生物学等方面的特点。方法使用雌性SD大鼠,随机分为假手术组和模型组,使用胫骨内注射法制成乳腺癌骨转移模型。造模后第19天时进行疼痛测定;第21天取材,测定肿瘤体积,通过影像技术评估骨质缺损程度,核医学测定骨矿物质含量(BMC)和骨密度(BMD),HE染色观察形态,抗酒石酸酸性磷酸酶(TRAP)染色并计数破骨细胞,免疫组化法测定增殖细胞核抗原(PCNA)、护骨素(OPG)和核因子kB受体活化因子配体(RANKL),荧光实时定量RT-PCR测定甲状旁腺激素相关蛋白(PTHrP)。结果模型组在造模后第19天已出现机械痛觉超敏、机械痛觉过敏和热痛觉过敏(P0.01)。第21天取材后胫骨影像评分升高(P0.01),BMD下降(P0.05);肉眼观察肿瘤生长明显(P0.01),镜下可见溶骨病变为主的混合性骨质破坏;破骨细胞数量和活性增加(P0.01),PTHrP、OPG水平与OPG/RANKL比值均下降(P0.05、P0.01),而RANKL无明显变化。结论乳腺癌骨转移大鼠模型具有疼痛和骨质破坏的表现,但未表现出PTHrP和RANKL升高,其损伤途径是通过抑制OPG破坏了OPG-RANKL-RANK系统的平衡,引起破骨细胞过度激活,造成骨吸收作用亢进。     

普瑞巴林对泰素诱导大鼠神经病理性疼痛治疗作用的研究

目的：研究普瑞巴林在泰素化疗所致大鼠神经病理性疼痛方面的治疗作用。方法：40只SD雄性大鼠随机分为正常对照组、普瑞巴林治疗组（30mg／kg,共16d,口服）、泰素治疗组（2mg／kg,隔日1次,共4次,腹腔给药）、低剂量普瑞巴林治疗组和高剂量普瑞巴林治疗组（泰素大鼠模型给予普瑞巴林10和30mg／kg,共16d,口服）共5组。给药第16天检测所有大鼠的机械性痛阈、热痛阂和冷痛阈,电镜检测大鼠坐骨神经。结果：与正常对照组相比,泰素能够产生机械性异常疼痛[（32．5±3．7）％vs（7．5±3．1）％,P〈0．01]、机械性痛觉过敏[（52．5±7．5）％VS（12．5±3．7）％,P〈0．01]、冷异常性疼痛[（2．9±0．5）Svs（0．5±0．3）S,P〈0．01]以及坐骨神经损伤,不伴有热痛觉过敏[（9．1±0．6）s vs（11．0±0．8）S,P〉0．053。而口服普瑞巴林（30mg／kg）连续16d能有效的降低泰素导致的神经病理性疼痛,与泰素组相比,它能减轻机械性痛觉异常[（12．5±3．7）％us（32．5±3．7）％,P〈0．013、机械性痛觉过敏[（30．0±3．8）％vs（52．5±7．5）％,P〈0．053、冷异常性疼痛[（1．4±0．3）Svs（2．9±0．5）S,P〈0．05]以及部分减轻坐骨神经损伤。结论：普瑞巴林能有效的减轻泰素化疗所致的神经病理性疼痛,可能是一种潜在有效的治疗化疗药物神经毒性的药物。     

地塞米松不同给药方式治疗大鼠放射性直肠炎疗效观察

目的:比较地塞米松分别采用腹腔注射及灌肠方式治疗大鼠放射性直肠炎的疗效.方法:32只SD大鼠随机分为4组:未放疗+生理盐水灌肠组(A组);放疗+生理盐水灌肠组 (B组);放疗+地塞米松灌肠组(C组);放疗+地塞米松腹腔注射组(D组).每组8只大鼠,除A组外所有大鼠盆腔均接受16.5Gy剂量的放疗.放疗10天后处死所有大鼠.直肠标本进行HE染色病理检查,并行肿瘤坏死因子-α(TNF-α)mRNA的RT-PCR检测,处死大鼠前抽大鼠静脉血行血清TNF-α的ELISA检测.结果:地塞米松灌肠并没有显示出治疗大鼠放射性直肠炎的作用,而地塞米松腹腔注射可以明显减轻大鼠直肠放射性炎症,并可以减少直肠局部TNF-α及血清TNF-α的表达.结论:地塞米松全身给药治疗放射性直肠炎是正确的给药方式.     

应用MADB-106乳腺癌细胞构建大鼠转移性骨癌痛模型

目的应用MADB-106大鼠乳腺癌细胞构建转移性骨癌痛模型,通过对该模型痛行为学、影像学、组织学观察等检测进行治疗研究。方法将MADB-106大鼠乳腺癌细胞接种到SD大鼠胫骨上段骨髓腔内,构建骨癌痛动物模型。以大鼠自发性缩足反射次数评估大鼠自发性痛情况,以自由活动时下肢跛行程度评分观察大鼠行走诱发痛,以热痛觉阈值观察大鼠热痛觉过敏情况,以X线、骨组织病理学检测观察癌细胞对骨结构的破坏程度。结果造模组大鼠术后第15天自发缩足反射次数为（14．42±1．24）次,第22天为（18．33±1．37）次,第25天为（21．25±1．54）次,与术前比较差异有统计学意义（均P〈0．001）;术后第15天热刺激痛觉阈值为（11．86±1．63）S,第22天为（8．38±1．05）S,第25天为（7．47±1．25）s（P〈0．001）;术后第15天自由行走痛评分为（1．25±0．62）分,第22天为（2．00±0．95）分,第25天为（2．33±1．07）分。术后第15天开始出现明显的自发性痛、热痛觉过敏和行走诱发痛,胫骨X线片显示明显的骨破坏,组织学研究显示骨髓腔内肿瘤生长,向外侵蚀破坏骨皮质。结论成功应用MADB-106乳腺癌细胞构建大鼠骨癌痛模型,造模2周后可以用于癌痛治疗的评价。     

何首乌有效成分对大鼠骨癌痛的镇痛效果

目的  探讨何首乌有效成分对大鼠骨癌痛的镇痛作用。方法 将36只SPF级雌性SD大鼠随机分成3组：A组为正常空白对照（n=6），B组大鼠注射无菌生理盐水（n=6），C组大鼠左后腿胫骨注射乳腺癌细胞walker256建立骨癌痛模型（n=24）。建立骨癌痛模型的C组SD大鼠按灌胃药物随机分成C1、C2、C3、C4 4组，每组6只。建模成功后14 d、15 d、16 d连续对C1~C4组大鼠分别灌胃生理盐水（2 mL）、二苯乙烯苷（60 mg/mL，2 mL）、大黄素（60 mg/mL，2 mL）和儿茶素（60 mg/mL，2 mL）。每次灌胃前、灌胃后30 min、灌胃后1.0 h测量大鼠左脚掌的机械痛阈值。结果 癌痛模型喂养第5天起，与A、B两组比较，C组大鼠机械痛阈值降低（P<0.05），骨质明显破坏；A、B两组大鼠机械痛阈值无明显差异，骨质结构正常。C2组大鼠各时点的机械性痛阈值均较C1组、C3组、C4组明显增加（P<0.05）。与灌胃前比较，C2组大鼠模型灌胃30 min和灌胃后1 h后机械性痛阈值明显升高（P<0.05），但灌胃30 min和灌胃后1 h后的机械性痛阈值无统计学意义（P>0.05）。结论 何首乌可有效降低大鼠的骨癌痛，其有效单体成分是二苯乙烯苷。     

神经生长因子对兔脊髓前角运动神经元保护作用的定量研究

钳夹损伤兔右坐骨神经，于损伤处注射蛇毒ＮＧＦ４００Ｂｕ／ｋｇ／日，损伤术后１，３，７天和２，３，４，６，８周动态观察脊髓腰段伤侧第ＩＸ板层外侧的大型运动神经元的ＡＣＰａｓｅ活性改变并应用图像分析仪对其进行定量研究。结果表明术后１，３天实验组和对照组ＡＣＰａｓｅ活性均增加；术后３周实验组ＡＣＰａｓｅ活性达高峰，溶酶体数目及溶酶体、高尔基复合体上的电子密度也明显增加，对照组酶活性不如实验组高，组间差异显著（Ｐ＜００１）。术后６周实验组ＡＣＰａｓｅ活性恢复至正常水平，而对照组ＡＣＰａｓｅ活性才开始回降。本研究显示蛇毒ＮＧＦ对坐骨神经损伤后脊髓前角运动神经元ＡＣＰａｓｅ活性恢复有促进作用，从而对运动神经元可起一定的保护和促进恢复的作用     

Effect of phenobarbital on plasma levels of cyclophosphamide and its metabolites in the mouse.

We have studied the quantitative pharmacokinetic differences of individual metabolites and unchanged cyclophosphamide (CPA) in control and phenobarbital-treated animals, using radiolabelled CPA together with thin-layer chromatography. On Day 0, one group was started on phenobarbital drinking water and one group stayed on regular acid water. P388 leukaemia, (10(6) cells i.p.) was administered to all mice on Day 8, and 2 days later both groups of mice were given i.p. CPA (200 mg/kg) with 14C-CPA (0.2 muCi per mouse). At 5--60 min after CPA administration, groups of 10 mice were killed and their blood collected for assay of parent compound and metabolites in plasma. Phenobarbital pretreatment reduced CPA and phosphoramide mustard CXT (concentration x time) by 66+% and 27+%, respectively. Assuming that phosphoramide mustard is both the ultimate cytotoxic form of CPA and the blood-transport form, the reduction of CPA by phenobarbital would predict a decreased therapeutic effect. The assay methods in this study will be used in the future to determine the importance of this potential drug interaction in man.     

Goshajinkigan reduces oxaliplatin-induced peripheral neuropathy without affecting anti-tumour efficacy in rodents

Oxaliplatin is a key drug in the treatment of colorectal cancer, but it causes acute and chronic neuropathies in patients. Goshajinkigan (GJG) is a Kampo medicine that is used for the treatments of several neurological symptoms including pain and numbness. More recently, GJG has been reported to prevent the oxaliplatin-induced peripheral neuropathy in clinical studies. No experimental study, however, has been conducted to date to determine the effect of GJG on pain behaviour in a rat model of oxaliplatin-induced neuropathy. Moreover, the impact on the anti-tumour effect of oxaliplatin remains unknown. In the present study, we examined the effects of GJG on the peripheral neuropathy and anti-tumour activity of oxaliplatin in rodents. Repeated administration of oxaliplatin caused cold hyperalgesia from days 3 to 37 and mechanical allodynia from days 21 to 28. Repeated administration of GJG prevented the oxaliplatin-induced cold hyperalgesia but not mechanical allodynia and axonal degeneration in rat sciatic nerve. Single administration of GJG reduced both cold hyperalgesia and mechanical allodynia after the development of neuropathy. In addition, GJG did not affect the anti-tumour effect of oxaliplatin in the tumour cells or tumour cells-implanted mice. These results suggest that GJG relieves the oxaliplatin-induced cold hyperalgesia and mechanical allodynia without affecting anti-tumour activity of oxaliplatin, and, therefore, may be useful for the oxaliplatin-induced neuropathy in clinical practice.     

糖皮质激素联合IFN-γ对肺纤维化小鼠的治疗作用及机制探讨

背景与目的： 观察糖皮质激素联合干扰素IFN-γ对肺纤维化小鼠的治疗作用。 材料与方法： 将雄性小鼠随机分为5组：阴性对照(生理盐水,NS)组、肺纤维化模型(博来霉素,BLM)组、地塞米松(DXM)治疗组、IFN-γ治疗组及DXM联合IFN-γ治疗组。后4组按3 mg/kg,气管内注入BLM建立肺纤维化模型,NS组采取相同手术方式,注入等量生理盐水。手术后1 d起,DXM组和联合组按 20 mg/kg皮下注射DXM,其余各组以相同方式给予生理盐水。从术后15 d起,IFN-γ组和联合组按0.01 μg/g皮下注射IFN-γ,其余各组以相同方式给予等量生理盐水。所有动物于术后22 d处死,显微镜下观察肺组织病理变化,取各组实验鼠肺组织匀浆液分别采用酸解法测定羟脯氨酸(Hyp)含量,免疫组化观察肿瘤坏死因子α (TNF-α) 的表达,荧光法测定还原型谷胱甘肽(GSH)与氧化型谷胱甘肽 (GSSG) 比值、丙二醛(MDA)含量以及总超氧化物歧化酶(T-SOD) 活性。 结果： DXM联合IFN-γ治疗组小鼠肺组织的病理评分与Hyp含量均低于BLM组及单独治疗组(P<0.05)。IFN-γ组小鼠肺组织的TNF-α表达最强,联合组的TNF-α表达介于DXM组和BLM组之间。联合组与BLM组及单独治疗组比较,GSH/GSSG升高,MDA含量减少,差异均有统计学意义(P<0.05)。各组之间,T-SOD活性的差异无统计学意义(P>0.05)。 结论： DXM与IFN-γ联合应用治疗小鼠肺纤维化效果明显优于单独用药。     

地塞米松对大鼠实验性神经根疼痛影响的时效性研究

目的采用行为药理学方法,探讨不同时期硬膜外地塞米松治疗对大鼠后足机械刺激疼痛阈值的影响,确定炎症和压迫因素的不同作用。方法取大鼠自体尾部椎间盘组织置于L5神经根下,建立椎间盘突出动物模型,然后硬膜外置管,采用早期预防性给药及晚期治疗性给药方法,观察地塞米松对大鼠后足底机械刺激疼痛阈值的影响。结果早期预防性硬膜外给予地塞米松完全抑制了大鼠2周内机械刺激疼痛阈值的降低,而3周时机械刺激阈值降到最低时治疗性硬膜外给予地塞米松对疼痛则无明显影响。结论椎间盘突出早期阶段,炎性反应是诱致疼痛的主要因素,硬膜外给予地塞米松可以抑制疼痛的产生;当椎间盘突出到达一定阶段,压迫因素成为致痛的主因时,硬膜外再给予地塞米松对已经产生的痛阈降低没有明显的缓解作用。     

Prevention of cisplatin-induced acute and delayed emesis by the selective neurokinin-1 antagonists,L-758,298 and MK-869

BACKGROUND: Recent studies have suggested that antiemetic therapy with a triple combination of the neurokinin-1 receptor antagonist MK-869, a serotonin (5-HT(3)) antagonist, and dexamethasone provides enhanced control of cisplatin-induced emesis compared with standard therapy regimens. The authors compared the antiemetic activity of a dual combination of MK-869 and dexamethasone with that of a standard dual combination of ondansetron and dexamethasone to characterize further the efficacy and tolerability profile of MK-869. METHODS: This was a multicenter, double-blind, randomized, active agent-controlled study of 177 cisplatin-na?ve patients with malignant disease. On Day 1, MK-869 was given intravenously as its water-soluble prodrug, L-758,298. Patients were randomized to one of three groups as follows. Group I received L-758,298 100 mg intravenously (i.v.), then dexamethasone 20 mg i.v., and cisplatin >or= 70 mg/m(2) on Day 1 followed by 300 mg MK-869 (tablet) orally on Days 2-5; Group II received L-758,298 100 mg i.v., then dexamethasone 20 mg i.v., and cisplatin >or= 70 mg/m(2) on Day 1 followed by placebo on Days 2-5; and Group III received ondansetron 32 mg i.v., then dexamethasone 20 mg i.v., and cisplatin >or= 70 mg/m(2) on Day 1 followed by placebo on Days 2-5. Emesis was recorded over Days 1-5 in a diary. Nausea was assessed every 24 hours by visual analog scale. Additional medication was available for emesis or nausea at any time. The primary efficacy parameters of interest were the proportion of patients without emesis and the proportion without emesis or rescue therapy on Day 1 (acute phase) and on Days 2-5 (delayed phase). RESULTS: No serious adverse events were attributed to L-758,298 or MK-869. On Day 1, the proportions of patients with no emesis and no use of rescue medication were 44% of patients in Group I, 36% of patients in Group II, 40% of patients in Groups I and II combined, and 83% of patients in Group III (P < 0.001 for Group III vs. the combined Groups I and II). The proportions of patients with no emesis and no use of rescue medication on Days 2-5 were 59% of patients in Group I, 46% of patients in Group II, and 38% of patients in Group III (P < 0.05 for Group I vs. Group III). The proportions of patients who were without emesis on Day 1 were 49% of patients in Group I, 47% of patients in Group II, and 84% of patients in Group III (P < 0.01 for Group I or II vs. Group III). On Days 2-5, however, the proportions of patients who were without emesis on Days 2-5 were 65% of patients in Group I, 61% of patients in Group II, and 41% of patients in Group III (P < 0.05 for Group I or II vs. Group III). Nausea scores in the acute phase were lower for Group III than for Group I, Group II, or Groups I and II combined (P < 0.05), although there was no significant difference among groups either for the delayed phase or overall for Days 1-5. CONCLUSIONS: Although the L-758,298 and dexamethasone combination reduced acute (Day 1) emesis compared with historic rates, dual therapy with ondansetron and dexamethasone was superior in controlling acute emesis. Continued dosing with MK-869 may enhance control of other measures of delayed emesis, such as the use of rescue medication, although confirmation is required before a definitive conclusion may be drawn. MK-869 given as dual therapy with dexamethasone was superior to ondansetron with dexamethasone for the control of delayed emesis (Days 2-5) and control of the need for rescue medication on Days 2-5.     

Comparative distribution of misonidazole and its amine metabolite in female Swiss Webster mice

The distribution of misonidazole and its terminal reduction product 1-(2-amino-1-imidazolyl)-3-methoxy-2-propanol (miso-amine) were compared in female Swiss Webster mice to determine if either misonidazole or miso-amine is distributed to peripheral nerves. Female Swiss Webster mice received a 100 mg/kg (5 microCi/mumole) i.p. dose of either 3H-misonidazole or 3H-miso-amine and the distribution of radioactivity was determined in various tissues including sciatic nerves and other myelinated nerves. Urine from misonidazole treated animals contained both miso-amine and misonidazole (8.4 and 20.4%, respectively, of the total radioactivity in the urine). Misonidazole produced higher initial tissue concentrations of radioactivity than did miso-amine. The relative tissue concentrations of radioactivity produced by misonidazole or miso-amine were similar, although not identical, 48 hours after administration of the drugs. Both sciatic and other myelinated nerves were found to retain radioactivity following the administration of either misonidazole or miso-amine.     

加巴喷丁预防长春新碱所致周围神经病理性疼痛的实验研究

目的探讨加巴喷丁（GBP）预防长春新碱致周围神经病理性疼痛的效果。方法将雌性KM小鼠80只随机分为4组（n=20）：空白对照组（NS组）、疼痛模型对照组（Pc组）、小剂量GBP实验组（S组）和大剂量GBP实验组（L组）。分别给予生理盐水、长春新碱、长春新碱＋小剂量GBP及长春新碱＋大剂量GBP。观察给药前后小鼠全身情况改变、热痛反应改变及给药后坐骨神经组织在光镜和电镜下组织形态和超微结构的改变。结果①全身情况：L组小鼠体重与Pc组比较,体重较为正常增长,差异有统计学意义（P〈0.05）。②热痛反应：与给药前基础值和NS组比较,Pc组热痛反应时间缩短,差异有统计学意义（P〈0.05）;与Pc组比较,L组给药后热痛反应时间延长,差异有统计学意义（P〈0.05）;③组织形态学改变：Pc组坐骨神经明显退行性变,神经细胞有脱髓鞘改变,部分施万细胞结构破坏,L组神经细胞均有神经结构改变,但程度比Pc组轻。结论加巴喷丁对预防长春新碱周围神经病理性疼痛有一定效果。     

神经损伤后NGF对骨骼肌纤维琥珀酸脱氢酶活性的影响

用持针器夹持兔右侧坐骨神经制作神经损伤动物模型。实验组动物于损伤处喷布蛇毒神经生长因子（ＮＧＦ）,对照组动物于同部位给予等量生理盐水,对胫骨前肌红肌、白肌和中间型肌纤维琥珀酸脱氢酶（ＳＤＨ）活性变化及分布进行定量、定位分析。结果显示,神经损伤１、２、３周,实验组和对照组各型肌纤维ＳＤＨ活性减弱,电镜下可见线粒体嵴断裂,酶阳性反应产物稀疏;神经损伤４周,实验组红肌、白肌和中间型肌纤维酶活性及分布恢复正常,对照组各型肌纤维酶活性仍较弱,电镜下酶阳性反应颗粒的分布也未恢复到正常水平。神经损伤３～６周,实验组各型肌纤维酶活性均强于对照组,组间差异显著（Ｐ＜００１）。本研究结果提示,坐骨神经损伤后,外源性的蛇毒ＮＧＦ对骨骼肌纤维酶活性和结构的恢复具有重要的促进作用