直肠扩张刺激引起IBS大鼠痛行为学以及骶髓DCN中神经元和胶质细胞的变化

目的采用行为学和免疫荧光化学的方法，观察直肠扩张刺激对IBS大鼠痛行为学以及大鼠骶髓后连合核（dorsal commissural nucleus，DCN）中神经元和胶质细胞的影响，为探讨IBS发生机制提供理论依据。方法动物分组：正常大鼠6只为空白对照组；感染旋毛虫的IBS大鼠42只，随机均分为7组：直肠放置气囊对照组、0．6ml组、0．8ml组、1．0ml组、1．2ml组、1．4ml组和1．5ml组。应用疼痛行为学的观察方法，观察1h各组动物的行为学改变，并采用免疫荧光化学的方法，观察大鼠DCN中神经元被激活的标志c-fos及胶质细胞的胶质原纤维酸性蛋白（glial fibrillary acidic protien，GFAP）和小胶质细胞特异性补体OX42的表达情况，空白对照组是在疼痛高峰点（1．2m1）处死取材。结果正常大鼠痛行为学积分在1．2ml组最为高，实验组IBS大鼠在0．8ml组的痛行为学最为明显，基本上达到痛行为学反应的高峰，可见IBS大鼠的痛阈值低于正常大鼠。对照组（1．2m1）中正常大鼠DCN中的c-fos、GFAP表达水平只相当于IBS中的0．8ml组的表达水平，低于1．0ml、1．2ml、1．4ml组；0X42的活化程度也较低只相当于IBS中的1．2ml组，并且明显低于1．4ml、1．5ml组。结论直肠扩张刺激明显引起IBS鼠痛行为的变化不但与骶髓中神经元活动存在密切关系，而且与神经胶质的活化可能也存在密切联系。     

老年大鼠脊髓腰骶段NADPH-d阳性体的表达及睾酮对其影响

目的探讨老年大鼠脊髓腰骶段还原型尼克酰胺腺嘌呤二核苷磷酸黄递酶(NADPH-d)阳性体的表达并观察睾酮对其的影响。方法健康雄性Wistar大鼠6月龄组、21月龄组和21月龄滴鼻组各5只;应用NADPH-d组织化学法检测大鼠脊髓腰骶段NADPH-d阳性体的表达,并观察老年大鼠鼻腔吸入睾酮后NADPH-d阳性体的影响。检测各月龄组大鼠切片后角浅层(SDH)、利绍尔束(LT)、中间外侧核(ILN)、骶髓后连合核(DCN)和中央管(CC)NADPH-d阳性体的数目。结果 6月龄组未出现NADPH-d阳性体,21月龄滴鼻组NADPH-d阳性体的表达明显少于21月龄组。结论老年大鼠鼻腔给予睾酮可以减少脊髓腰骶段NADPH-d阳性体表达。     

结肠炎诱导大鼠行为学变化及骶髓后连合核和丘脑板内核群中GFAP表达的意义

目的探讨因福尔马林引起的大鼠急性结肠炎刺激诱导的行为学变化及骶髓后连合核(dorsal commissural nucleuse,DCN)和丘脑板内核群(thalamic intralaminar nuclei,ILN)胶质原纤维酸性蛋白(glial fibrillary acidic protein,GFAP)的表达及其意义。方法给大鼠乙状结肠注射5%的福尔马林100μL制作急性结肠炎引发内脏痛大鼠模型。采用痛行为学积分方法观察不同时间点急性结肠炎大鼠行为学变化。采用免疫组织化学方法,观察不同时间点急性结肠炎大鼠骶髓后连合核和丘脑板内核GFAP表达变化情况。结果急性结肠炎大鼠痛行为表现高峰为造模后60 min,90 min时减低程度显著。GFAP在骶髓后连合核的表达在造模形成后的45 min最为明显,在90 min明显降低。而在丘脑板内核的表达60 min最为明显,120 min明显降低。结论大鼠痛行为学的变化是由于急性炎症引起的内脏痛而导致,与疼痛变化密切相关的胶质细胞中GFAP在脊髓内反应早且明显,而在与情绪变化密切相关的丘脑内的板内核群中变化相对较晚。     

大鼠小脑颗粒神经元体外原代培养

目的 体外原代培养大鼠小脑颗粒神经元,为研究慢性砷暴露对小脑神经元的毒性作用提供实验方法.方法 取生后5～7天Wistar仔鼠,体式显微镜下分离小脑皮层,0.25％胰蛋白酶消化、DNA Ⅰ酶洗涤制成单细胞悬液,两次差速贴壁后接种在多聚赖氨酸包被的培养板内,相差镜下观察大鼠小脑颗粒神经元成长、发育变化及突触形成.采用神经元特异性烯醇化酶(NSE)免疫荧光技术鉴定神经元.结果 培养后第24小时,相差显微镜下可见大鼠小脑颗粒神经元贴壁,呈网状排列;第2～3天,神经元胞体由椭圆形变成圆形,轮廓逐渐清晰,细胞伸出突起,突起逐渐延长,细胞间通过突起连接,形成了稀疏的神经元突触网络;第4～6天,细胞体积进一步增大,细胞间通过广泛的突触联系,神经元清晰饱满,形成了复杂的神经元网络.共聚焦显微镜下,可见大量含NSE的神经元.结论 成功地进行了大鼠小脑颗粒神经元的原代培养,该方法可为今后研究慢性砷暴露对小脑细胞的毒性作用提供实验依据.     

成年大鼠神经元和星形胶质细胞细胞周期蛋白依赖激酶的表达

目的 研究成年大鼠细胞周期蛋白依赖激酶（CDK）在神经元和星型胶质细胞的表达.方法 应用免疫荧光和激光扫描共聚焦显微镜观察成年大鼠生理状态下大脑皮层或海马CA1区神经元和星型胶质细胞CDK1、CDK2、CDK4的表达.结果 成年大鼠大脑皮层和海马CA1区神经元的细胞核和细胞浆均有CDK1、CDK2和CDK4表达,以胞核为主;星形胶质细胞也有CDK1、CDK2和CDK4的表达,但表达细胞数目较少,且表达这些指标的星形胶质细胞多聚集在海马CA1区.结论 成年大鼠大脑皮层和海马区的神经元和星形胶质细胞均表达CDK,而神经元的CDK表达较星形胶质细胞更为普遍.     

TREM2对小胶质细胞的免疫调控在缺血性卒中中的作用

缺血性卒中是一种常见的神经系统疾病, 可导致神经元死亡和神经功能障碍。小胶质细胞是中枢神经系统的主要免疫细胞, 参与卒中后炎症和组织修复。髓样细胞表达的触发受体2(triggering receptor expressed on myeloid cells 2, TREM2)是一种在小胶质细胞表面表达的受体, 在缺血性卒中后神经元存活和神经修复方面发挥着多方面的作用, 包括促进小胶质细胞的吞噬作用、抑制过度的炎症反应、维持小胶质细胞的增殖和存活、保护神经元免受损伤以及促进神经功能恢复。因此, 阐明脑缺血后TREM2对小胶质细胞的免疫调节机制, 对于探索缺血性卒中新的治疗方向具有重要意义。     

白介素-1β和小胶质细胞在帕金森病中的作用

目的 探讨白介素-1β(IL-1β)和小胶质细胞在帕金森病(PD)发病机制中的作用,阐述小胶质细胞激活后作用的可能合理模式.方法 采用立体定向术将嗜神经毒素6-羟基多巴(6-OHDA)注入大鼠右侧纹状体制作偏侧PD大鼠模型.造模2个月后,计数黑质致密部神经元和小胶质细胞数目,采用免疫组织化学方法观察黑质致密部IL-1β表达水平的变化.结果 光镜下观察模型组右侧黑质致密部多巴胺能神经元几乎消失,小胶质细胞数目明显增多,与假手术组和正常对照组相比,差异有统计学意义(P＜0.05).免疫组化染色显示模型组右侧黑质致密部可见明显的小胶质细胞核周有IL-1β的表达,呈棕褐色;而模型组左侧黑质、假手术组和正常对照组右侧黑质未见明显的IL-1β的表达.结论 嗜神经毒素6-OHDA可导致神经元释放小胶质细胞激活态物质,激活的小胶质细胞释放IL-1β介导细胞毒性作用促进神经元的慢性变性坏死.     

脊髓损伤大鼠远端神经元及骨骼肌变化的实验研究

目的探讨脊髓损伤大鼠远端神经元及骨骼肌变化情况,以期为临床上治疗提供有效依据。方法选取30只大鼠为研究对象,每组10只,分别为对照组、手术组和脊髓损伤组。对照组为正常大鼠,手术组行椎板切除术,脊髓损伤组行胸10完全脊髓损伤。在制成模型后1周、2周、4周、12周、24周观察大鼠坐骨神经-运动终板-内侧腓肠肌形态变化情况。结果脊髓损伤电镜下坐骨神经术后12周有髓神经纤维髓鞘崩解,崩解髓鞘板层清晰,术后24周有髓神经纤维髓鞘已模糊、碎裂髓鞘增多,薄髓和无髓神经纤维12周后增多;腓肠肌光镜下术后12周局部肌细胞边界清楚,多数模糊,肌细胞核相对聚集,结缔组织增生明显;术后24周肌细胞融合,细胞核密集,融合细胞间见有空隙,结缔组织增生明显;电镜下运动终板术后12周突触皱褶和突触前后膜不可辨,突触结构紊乱,肌纤维明暗带清晰,z线不连续,高倍镜下突触皱褶未见,突触前后膜不可辨,可见类圆形突触小泡和细小颗粒,肌板结构清晰。结论大鼠脊髓损伤后在损伤平面以下周围神经、运动终板、骨骼肌在形态上会发生规律性变化,12周后显著变化,24周后则毁损性改变。     

2%氢气生理盐水对阿尔茨海默病大鼠海马神经细胞的保护作用

目的探讨2%氢气生理盐水治疗的阿尔茨海默病(AD)大鼠学习、记忆能力以及海马神经元及神经胶质细胞的形态学变化的影响。方法雄性SD大鼠,随机分为正常对照组、生理盐水治疗组及2%氢气生理盐水治疗组,每组各10只。按6 mg/kg腹腔注射三甲基锡(TMT)诱导AD大鼠模型。按10 ml/kg腹腔注射2%氢气生理盐水进行治疗,生理盐水治疗组按同样剂量进行注射。Morris水迷宫实验检测大鼠空间学习、记忆能力,尼氏染色观察大鼠海马神经元数量及尼氏小体的变化,免疫组织化学检测caspase-3在海马神经元的表达,电镜观察海马神经元及胶质细胞超微结构的变化。结果 2%氢气生理盐水能显著改善AD大鼠空间学习、记忆能力障碍,抑制caspase-3的表达活性,降低海马神经元的凋亡,保护神经元,同时电镜检测显示海马神经元及胶质细胞的超微结构得到改善。结论 2%氢气生理盐水能够改善海马神经元及胶质细胞的超微结构,抑制细胞凋亡,保护神经组织,从而提示2%氢气生理盐水对AD有保护治疗作用,其深层机制有待进一步探讨。     

小胶质细胞在偏头痛大鼠中枢敏化过程中的作用

目的观察二甲胺四环素(MC)对偏头痛大鼠痛觉超敏行为、颈髓后角小胶质细胞及神经元激活的影响,探讨小胶质细胞在偏头痛大鼠模型中枢敏化过程中的作用。方法 66只雄性SD大鼠随机分为空白组、假手术组、生理盐水组(NS组)、新型致炎剂(IS)4d组(IS4组)、IS 7d组(IS7组)、IS/MC预防组、IS/NS预防组、NS/NS预防组、IS/MC治疗组、IS/NS治疗组、NS/NS治疗组。每组6只。采用Vonfrey纤维丝测定各组大鼠眶周痛觉阈值,免疫荧光染色测定颈髓后角小胶质细胞及神经元激活情况。结果硬脑膜给予IS第3天眶周痛觉阈值较NS组明显下降(P<0.01)。IS/MC预防组眶周痛觉阈值明显高于IS/NS预防组(P<0.01)。IS4组、IS7组小胶质细胞平均荧光密度值高于假手术组(P<0.01)。IS/MC预防组、IS/MC治疗组小胶质细胞平均荧光密度值分别低于IS/NS预防组、IS/NS治疗组(P<0.01)。IS/MC预防组C-fos平均荧光密度值明显低于IS/NS预防组(P<0.01)。结论在慢性硬脑膜炎症所致的中枢敏化过程中小胶质细胞可能仅在启动阶段起作用,对于痛觉超敏的维持无作用。MC能有效预防偏头痛大鼠模型痛觉超敏的发生,但对已存在的痛觉超敏无治疗作用。     

Estrogen receptor beta is essential for sprouting of nociceptive primary afferents and for morphogenesis and maintenance of the dorsal horn interneurons

Estrogen is known to influence pain, but the specific roles of the two estrogen receptors (ERs) in the spinal cord are unknown. In the present study, we have examined the expression of ERalpha and ERbeta in the spinal cord and have looked for defects in pain pathways in ERbeta knockout (ERbeta(-/-)) mice. In the spinal cords of 10-month-old WT mice, ERbeta-positive cells were localized in lamina II, whereas ERalpha-positive cells were mainly localized in lamina I. In ERbeta(-/-) mice, there were higher levels of calcitonin gene-regulated peptide and substance P in spinal cord dorsal horn and isolectin B4 in the dorsal root ganglion. In the superficial layers of the spinal cord, there was a decrease in the number of calretinin (CR)-positive neurons, and in the outer layer II, there was a loss of calbindin-positive interneurons. During embryogenesis, ERbeta was first detectable in the spinal cord at embryonic day 13.5 (E13.5), and ERalpha was first detectable at E15.5. During middle and later embryonic stages, ERbeta was abundantly expressed in the superficial layers of the dorsal horn. ERalpha was also expressed in the dorsal horn but was limited to fewer neurons. Double staining for ERbeta and CR showed that, in the superficial dorsal horn of WT neonates [postnatal day 0 (P0)], most CR neurons also expressed ERbeta. At this stage, few CR-positive cells were detected in the dorsal horn of ERbeta(-/-) mice. Taken together, these findings suggest that, early in embryogenesis, ERbeta is involved in dorsal horn morphogenesis and in sensory afferent fiber projections to the dorsal horn and that ERbeta is essential for survival of dorsal horn interneurons throughout life.     

Spinal neurons exhibiting a specific nociceptive response receive abundant substance P-containing synaptic contacts.

Substance P has been implicated in nociceptive transmission in the spinal cord. However, evidence for a direct correlation between a specific nociceptive response in spinal dorsal horn neurons and substance P input is lacking. In this study, we combine intracellular recording from dorsal horn neurons in vivo, characterization of their nociceptive responses, intracellular labeling by injection of horseradish peroxidase, and immunocytochemical demonstration of substance P at the electron microscopic level. The results reveal that dorsal horn neurons that respond to noxious cutaneous stimulation with a slow, prolonged excitatory postsynaptic potential receive a preferentially high number of substance P fibers compared with nonnociceptive neurons, which scarcely receive any substance P input. Therefore, this study provides direct evidence of a structural-functional link for a substance P-mediated nociceptive response.     

Immunohistochemical analysis of peptide pathways possibly related to pain and analgesia: enkephalin and substance P.

The distribution of Met-enkephalin- and substance P-immunoreactive neurons was studied by indirect immunofluorescence in some areas related to pain and analgesia. Met-enkephalin- and substance P-positive cell bodies and nerve terminals were observed in the periaqueductal central gray, the nucleus raphe magnus, the marginal layers and substantia gelatinosa of the spinal trigeminal nucleus, and the dorsal horn of the spinal cord. Lesion experiments suggest that Met-enkephalin neurons in the dorsal horn and possibly in the spinal trigeminal nucleus are interneurons or propriospinal neurons with nerve terminals in the laminae I and II of the cord and in the superficial layers of the spinal trigeminal nucleus, respectively. These areas are also very rich in substance P-positive nerve terminals, mainly representing central branches of primary afferent neurons. The present immunohistochemical-anatomical findings support the hypothesis that stimulation-produced analgesia is related to activation of spinal and spinal trigeminal enkephalin interneurons forming axo-axonic synapses with (substance P?) pain afferents in the superficial laminae of the dorsal horn and the spinal trigeminal nucleus. These interneurons may be activated by sensory fibers and by descending fibers from medullary stimulation sites. Transmitter substances in these descending fibers may be 5-hydroxytryptamine and substance P.     

IFN-γ receptor signaling mediates spinal microglia activation driving neuropathic pain

Neuropathic pain, a highly debilitating pain condition that commonly occurs after nerve damage, is a reflection of the aberrant excitability of dorsal horn neurons. This pathologically altered neurotransmission requires a communication with spinal microglia activated by nerve injury. However, how normal resting microglia become activated remains unknown. Here we show that in naive animals spinal microglia express a receptor for the cytokine IFN-γ (IFN-γR) in a cell-type-specific manner and that stimulating this receptor converts microglia into activated cells and produces a long-lasting pain hypersensitivity evoked by innocuous stimuli (tactile allodynia, a hallmark symptom of neuropathic pain). Conversely, ablating IFN-γR severely impairs nerve injury-evoked microglia activation and tactile allodynia without affecting microglia in the contralateral dorsal horn or basal pain sensitivity. We also find that IFN-γ-stimulated spinal microglia show up-regulation of Lyn tyrosine kinase and purinergic P2X₄ receptor, crucial events for neuropathic pain, and genetic approaches provide evidence linking these events to IFN-γR-dependent microglial and behavioral alterations. These results suggest that IFN-γR is a key element in the molecular machinery through which resting spinal microglia transform into an activated state that drives neuropathic pain.     

Effects of tegaserod on Fos, substance P and calcitonin gene-related peptide expression induced by colon inflammation in lumbarsacral spinal cord

AIM: To investigate the mechanisms of tegaserod, a partial 5-HT4 agonist, in reducing visceral sensitivity by observing Fos, substance P (SP) and calcitonin gene-related peptide (CGRP) expression in the lumbarsacral spinal cord induced by colonic inflammation in rats. METHODS: Twenty-four male rats with colonic inflammation induced by intraluminal instillation of trinitrobenzenesulfonic acid (TNBS) were divided into 3 groups. Treatment group 1: intra-gastric administration of tegaserod, 2 mg/kg.d; Treatment group 2: intra-gastric administration of tegaserod, 1 mg/kg.d; Control group: intra-gastric administration of saline, 2.0 mL/d. After 7 d of intra-gastric administration, lumbarsacral spinal cord was removed and processed for Fos, SP and CGRP immunohistochemistry. RESULTS: In rats of the control group, the majority of Fos labeled neurons was localized in deeper laminae of the lumbarsacral spinal cord (L(5)-S(1)). SP and CGRP were primarily expressed in the superficial laminae of the spinal cord after TNBS injection. Intra-gastric administration of tegaserod (2 mg/kg.d) resulted in a significant decrease of Fos labeled neurons (22.0+/-7.7) and SP density (12.5+/-1.4) in the dorsal horn in the lumbarsacral spinal cord compared to those of the control group (62.2+/-18.9, 35.9+/-8.9, P<0.05). However, CGRP content in dorsal horn did not significantly reduce in rats of treatment group 1 (1.2+/-1.1) compared to that of the control group (2.8+/-2.4, P>0.05). Neither Fos expression nor SP or CGRP density in the dorsal horn significantly declined in rats of treatment group 2 compared to those of the control group (P>0.05). CONCLUSION: Tegaserod can significantly reduce Fos labeled neurons in the lumbarsacral spinal cord induced by colonic inflammation. Tegaserod may reduce visceral sensitivity by inhibiting SP expression in the dorsal horn of spinal cord.     

Glutamate and substance P coexist in primary afferent terminals in the superficial laminae of spinal cord

By light microscopic immunocytochemistry it has been previously shown that approximately equal to 70% of the neurons in rat dorsal root ganglia are labeled with an antiserum for glutamate conjugated to hemocyanin; the smaller among these neurons are also positive for substance P. By using a postembedding ImmunoGold method and electron microscopy, it is shown here that synaptic terminals in the superficial laminae of the spinal cord of rats selectively stain for the same glutamate antiserum. Immunolabeling is in small dome-shaped and in large scalloped synaptic terminals. Scalloped terminals are of two types. One type consists of dark terminals with many agranular vesicles of different size and a few large granular vesicles; these are probably endings of unmyelinated and small myelinated primary afferent fibers. The other type consists of light terminals with small agranular vesicles homogeneous in size with neurofilaments and many mitochondria; these are probably endings of larger myelinated primary afferent fibers. By means of double-labeling electron microscopic immunocytochemistry with colloidal gold particles of two different sizes, it is also shown here that substance P is present in only the dark type of glutamate-labeled scalloped terminals. The primary afferent origin of the terminals labeled by the antisera for glutamate and for substance P is demonstrated by a triple-labeling strategy: immunocytochemistry for both antisera on sections from rats in which dorsal rhizotomy or dorsal root ganglion injection of horseradish peroxidase conjugated to wheat germ agglutinin was performed. It is proposed that glutamate is the neurotransmitter in primary afferents mediating input from different peripheral receptor classes, including nociceptors. Effects of glutamate and substance P on spinal dorsal horn neurons may result from co-release of these two mediators from the same dorsal root afferent terminal.     

Differential distribution of two ATP-gated channels (P2X receptors) determined by immunocytochemistry.

Several P2X receptor subunits were recently cloned; of these, one was cloned from the rat vas deferens (P2X1) and another from pheochromocytoma (PC12) cells differentiated with nerve growth factor (P2X2). Peptides corresponding to the C-terminal portions of the predicted receptor proteins (P2X1 391-399 and P2X2 460-472) were used to generate antisera in rabbits. The specificities of antisera were determined by staining human embryonic kidney cells stably transfected with either P2X1 or P2X2 receptors and by absorption controls with the cognate peptides. In the vas deferens and the ileal submucosa, P2X1 immunoreactivity (ir) was restricted to smooth muscle, whereas P2X2-ir was restricted to neurons and their processes. Chromaffin cells of the adrenal medulla and PC12 cells contained both P2X1- and P2X2-ir. P2X1-ir was also found in smooth muscle cells of the bladder, cardiac myocytes, and nerve fibers and terminals in the superficial dorsal horn of the spinal cord. In contrast, P2X2-ir was observed in scattered cells of the anterior pituitary, neurons in the hypothalamic arcuate and paraventricular nuclei, and catecholaminergic neurons in the olfactory bulb, the substantia nigra, ventral tegmental area, and locus coeruleus. A plexus of nerve fibers and terminals in the nucleus of the solitary tract contained P2X2-ir. This staining disappeared after nodose ganglionectomy, consistent with a presynaptic function. The location of the P2X1 subunit in smooth muscle is consistent with its role as a postjunctional receptor in autonomic transmission, while in neurons, these receptors appear in both postsynaptic and presynaptic locations.     

Anatomical and physiological evidence for involvement of tuberoinfundibular peptide of 39 residues in nociception

The parathyroid hormone 2 (PTH2) receptor's anatomical distribution suggests that, among other functions, it may be involved in modulation of nociception. We localized PTH2 receptor protein to spinal cord lamina II and showed that it is synthesized by subpopulations of primary sensory neurons and intrinsic spinal cord dorsal horn neurons. Tuberoinfundibular peptide of 39 residues (TIP39) selectively activates the PTH2 receptor. Intraplantar microinjection of TIP39 caused a paw-withdrawal response and intrathecal injection caused scratching, biting, and licking, a nocifensive response. Intrathecal administration of a TIP39 antibody decreased sensitivity in tail-flick and paw-pressure assays. Intrathecal administration of TIP39 potentiated responses in these assays. We determined the sequence of TIP39's precursor and found that mRNA encoding TIP39 and TIP39-like immunoreactivity is concentrated in two brainstem areas, the subparafascicular area and the caudal paralemniscal nucleus. Cells in these areas project to the superficial dorsal horn of the spinal cord. Our data suggest that TIP39 released from supraspinal fibers potentiates aspects of nociception within the spinal cord.     

丝胶对糖尿病大鼠脊髓及脊神经节细胞神经生长因子表达的作用

目的 探讨丝胶对2型糖尿病大鼠脊髓及脊神经节细胞神经生长因子(NGF)表达的作用.方法 36只雄性SD大鼠,随机分为正常对照组、糖尿病模型组和丝胶治疗组(n=12).采用SP法观察坐骨神经对应脊髓节段(L4～6)和脊神经节细胞NGF蛋白的表达.结果 NGF蛋白免疫阳性产物为棕黄色细腻颗粒状,位于脊神经节细胞和脊髓前角细胞的胞质和胞核,以胞质为主.与正常对照组大鼠比较,糖尿病模型组大鼠脊髓前角细胞和脊神经节细胞NGF蛋白的表达明显降低(P＜0.01);与糖尿病模型组大鼠比较,丝胶治疗组大鼠脊髓前角细胞、脊神经节细胞NGF蛋白的表达明显升高(P＜0.01).结论 丝胶上调脊髓前角细胞和脊神经节细胞NGF的表达,保护糖尿病坐骨神经相关神经元胞体.