Soluble p75 neurotrophic receptor as a reliable biomarker in neurodegenerative diseases: what is the evidence?

Neurodegenerative diseases are often misdiagnosed,especially when the diagnosis is based solely on clinical symptoms.The p75 neurotrophic receptor(p75^(NTR))has been studied as an index of sensory and motor nerve development and maturation.Its cleavable extracellular domain(ECD)is readily detectable in various biological fluids including plasma,serum and urine.There is evidence for increased p75NTR ECD levels in neurodegenerative diseases such as Alzheimer’s disease,amyotrophic lateral sclerosis,age-related dementia,schizophrenia,and diabetic neuropathy.Whether p75^(NTR) ECD could be used as a biomarker for diagnosis and/or prognosis in these disorders,and whether it could potentially lead to the development of targeted therapies,remains an open question.In this review,we present and discuss published studies that have evaluated the relevance of this emerging biomarker in the context of various neurodegenerative diseases.We also highlight areas that require further investigation to better understand the role of p75^(NTR) ECD in the clinical diagnosis and management of neurodegenerative disorders.

GDI2通过p75NTR通路调节结直肠癌细胞增殖、迁移、侵袭和凋亡

目的:探讨GDP解离抑制因子2(GDI2)对结直肠癌(CRC)细胞增殖、迁移、侵袭和凋亡以及细胞周期的影响及其机制。方法:TCGA数据库分析GDI2 mRNA在CRC肿瘤组织中的表达。将CRC细胞分为sh-NC组和sh-GDI2组,采用CCK-8法检测细胞活力,克隆形成实验检测细胞增殖,Transwell实验检测细胞迁移和侵袭,流式细胞术检测细胞凋亡和周期,实时荧光定量PCR(RT-qPCR)检测GDI2基因表达,western blotting检测GDI2蛋白和神经生长因子受体(p75NTR)通路关键因子(IKK、p-NF-κB和p-IκB)的表达。构建异种移植瘤裸鼠模型,观察GDI2对CRC肿瘤生长的影响。结果:与癌旁正常组织和正常结肠上皮细胞相比,GDI2在CRC患者肿瘤组织和细胞系中的表达上调(P<0.05)。sh-GDI2能抑制CRC细胞增殖、迁移、侵袭,阻滞细胞周期进程,并促进凋亡(均P<0.05)。与sh-NC组相比,sh-GDI2组p75NTR蛋白表达上调,IKK、p-NF-κB、p-IκB蛋白表达下调(均P<0.05)。敲低GDI2可明显抑制裸鼠体内CRC肿瘤的生长(P<0.05)。结论:敲低GDI2可能通过p75NTR信号通路抑制CRC细胞增殖、侵袭和迁移,促进细胞凋亡。

Role of the nerve growth factor precursor-neurotrophin receptor p75 and sortilin pathway on apoptosis in the brain of patients with intracerebral hemorrhage

This study demonstrated that brain areas surrounding the site of hematoma following intracerebral hemorrhage are characterized by significantly increased apoptosis and expression of neurotrophin receptor p75 and sortilin. However, as detected by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemical staining, there was no significant change in nerve growth factor precursor expression levels. The appearance of neurotrophin receptor p75 expressing cells was positively correlated with cells that were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. These findings confirm that the nerve growth factor precursor-neurotrophin receptor p75-sortilin heterotrimeric complex-mediated apoptosis pathway may play an important role in cellular apoptosis following intracerebral hemorrhage.

Association between p75 neurotrophin receptor gene expression and cell apoptosis in tissues surrounding hematomas in rat models of intracerebral hemorrhage

Animal models of intracerebral hemorrhage were established by injection of autologous blood into the caudate nucleus in rats. Cell apoptosis was measured by flow cytometry and immunohistochemical staining of the p75 neurotrophin receptor. p75 neurotrophin receptor protein was detected by immunohistochemistry. p75 neurotrophin receptor mRNA was examined by quantitative real-time polymerase chain reactions. At 24 hours after modeling, cellular apoptosis occured around hematoma with upregulation of p75 neurotrophin receptor protein and mRNA was observed, which directly correlated to apoptosis. This observation indicated that p75 neurotrophin receptor upregulation was associated with cell apoptosis around hematomas after intracerebral hemorrhage.

Towards a comprehensive understanding of p75 neurotrophin receptor functions and interactions in the brain

The role of neurotrophins in neuronal plasticity has recently become a strong focus in neuroregeneration research field to elucidate the biological mechanisms by which these molecules modulate synapses,modify the response to injury,and alter the adaptation response.Intriguingly,the prior studies highlight the role of p75 neurotrophin receptor(p75^(NTR))in various injuries and diseases such as central nervous system injuries,Alzheimer's disease and amyotrophic lateral sclerosis.More comprehensive elucidation of the mechanisms,and therapies targeting these molecular signaling networks may allow for neuronal tissue regeneration following an injury.Due to a diverse role of the p75^(NTR)in biology,the body of evidence comprising its biological role is diffusely spread out over numerous fields.This review condenses the main evidence of p75^(NTR)for clinical applications and presents new findings from published literature how data mining approach combined with bioinformatic analyses can be utilized to gain new hypotheses in a molecular and network level.

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.

p75 neurotrophin receptor signal pathway influence on apoptosis in anterior horn neurons of the spinal cord in a rat model of cauda equina compression injury

BACKGROUND： Studies have demonstrated that cauda equina compression results in apoptosis of motor neurons in the spinal cord. The combination of p75 neurotrophin receptor （p75NTR） and precursor of nerve growth factor （pro-NGF） expression initiates the apoptotic pathway and induces neuronal apoptosis. However, few reports have focused on the p75-mediated mechanism of neuronal apoptosis following cauda equine compression injury OBJECTIVE： To determine apoptosis of spinal cord neurons and activation of the pro-NGF-p75NTR-JNK（c-Jun N-terminal kinase） signal pathway in rats following cauda equina compression, and to verify experimental outcomes. DESIGN, TIME AND SETTING： A randomized, controlled, in vivo experiment was performed at the Medical Experimental Center of Xi＇an Jiaotong University between April and November in 2008. MATERIALS： Streptavidin-perosidase kit was purchased from Wuhan Boster, China; in situ end labeling detection kit was provided by Promega, USA; type AEG-220G electron microscope was purchased from Hitachi, Japan. METHODS： A total of 48 healthy, adult, female, Sprague Dawley rats were randomly assigned to three groups： normal （n = 6）, sham-surgery （n = 6）, and compression （n = 36）. The compression group was randomly assigned to six subsets at 1,3, 5, 7, 14, and 28 days, respectively, with 6 rats in each subset. A cylindrical silica gel stick was implanted into the rats to compress 75% of the vertebral canal in the compression group; in the sham-surgery group, only vertebral resection was performed; and no procedures were performed in the normal group. MAIN OUTCOME MEASURES： At 1,3, 5, 7, 14, and 28 days following compression, L2-3 spinal cord segments were processed for immunohistochemistry, in situ cell apoptosis detection, and transmission electron microscopy observation. Nissl staining was used to observe neuronal survival in the L2 spinal cord segment. Immunohistochemistry was applied to detect expressions of pro-NGF, p75NTR, and JNK in the L2 segment. TUNEL fluorometric method was used to observe apoptosis of neurons in the L2 segment. RESULTS： In the normal and sham-surgery groups, little neuronal apoptosis was observed in the L2-3 spinal cord segment. At 3 days after compression injury, pro-NGF, p75NTR and JNK expression was observed in the spinal cord. Expression levels reached a peak at 7 days, and then gradually decreased. In the compression and sham-surgery groups, neurons primarily expressed pro-NGF and p75NTR. The number of JNK-positive neurons in the compression group was dramatically increased compared with the sham-surgery group （P〈 0.05）. A few neurons were apoptotic in the spinal cord 1 day after compression injury. The number of apoptotic neurons gradually increased and reached a peak at 7 days, and subsequently decreased. Apoptosis was still detectable at 28 days. There was a positive correlation between p75NTR expression and neuronal apoptosis （r= 0.75, P〈 0.05）. CONCLUSION： Following cauda equina compression injury, apoptosis of spinal cord neurons was observed. The compression-induced neuronal apoptosis was associated with p75NTR expression in the L2-3 spinal cord segment.

红景天苷对阿尔茨海默病模型大鼠学习记忆能力和海马组织Aβ含量及p75NTR表达的影响

目的探讨红景天苷对Aβ1~40所致阿尔茨海默病(AD)模型大鼠学习记忆能力,p75NTR信号通路关键蛋白表达和β-淀粉样蛋白(Aβ)含量的影响。方法选取96只雄性SD大鼠,随机分为假手术组,模型对照组,红景天苷小、中、大剂量组,石杉碱甲组,每组16只。除假手术组外,各组大鼠均于双侧海马CA1区缓慢注射Aβ1~40各1μL(10μg)制备AD大鼠模型,假手术组则注射等量0.9%氯化钠溶液。红景天苷小、中、大剂量组分别于术后24 h灌胃红景天苷25,50,100 mg·kg^(-1),石杉碱甲组给予灌胃石杉碱甲50 mg·kg^(-1),假手术组及模型对照组灌胃等量0.9%氯化钠溶液,共21 d。给药结束后经Morris水迷宫实验观察红景天苷对模型大鼠学习记忆能力的影响,并采用酶联免疫吸附测定(ELISA)法检测大鼠血清与海马组织中Aβ的含量,免疫组化法检测海马区神经元中p75NTR和p-JNK蛋白表达。结果与模型对照组比较,红景天苷小、中、大剂量组大鼠在水迷宫训练中潜伏期明显缩短(P<0.05或P<0.01),而水迷宫测试中跨越平台的次数显著增加(P<0.05或P<0.01);红景天苷小、中、大剂量组血清与海马组织中Aβ含量显著降低;海马神经元p75NTR、p-JNK表达显著减少(P<0.05或P<0.01)。结论红景天苷可改善Aβ1~40所致学习记忆障碍模型大鼠学习记忆能力,其作用机制可能与其抑制p75NTR对Aβ的调控通路,减少Aβ的神经毒性作用,从而使海马神经细胞凋亡减少有关。

脑出血血肿周围组织中P75NTR和proNGF的表达及其与细胞凋亡的关系

目的:通过对人脑出血后血肿周围不同区域组织中的P75NTR及proNGF表达的检测,探讨其在脑出血后血肿周围组织细胞凋亡中的作用。方法:本实验采集脑出血血肿清除术患者的脑组织标本,分别运用DNA断裂原位末端标记(TUNEL)法检测血肿周围及远隔部位组织中凋亡细胞、免疫组化技术及WesternBlot检测P75NTR及proNGF的表达。结果:相对于远隔部位组织,脑出血后血肿周围组织中的细胞凋亡率与P75NTR的表达水平明显增加(P<0.01),而proNGF的表达水平并没有显著变化(P>0.05),P75NTR的阳性细胞率与TUNEL的阳性细胞率呈正相关(R=0.628,P=0.00)。结论:脑出血后,血肿周围组织与远隔的组织相比,细胞凋亡数量明显增多,与此相对应,P75NTR的表达显著增高。至于proNGF的表达量并没有很大变化,则是因为多大比例的proNGF被裂解为mNGF可能决定了是以proNGF发挥凋亡作用还是以mNGF形式发挥促进存活作用,或是因为细胞膜表面P75NTR的表达增加,使更多的proNGF与P75NTR相结合,大量结合的proNGF由于内化的因素而不易被检测。

钼对人食管癌细胞ECA-109的化疗增敏作用及对食管癌干细胞p75^(NTR)的影响

目的:探讨钼对食管癌细胞ECA-109化疗敏感性的影响及对食管癌干细胞p75NTR作用.方法:本实验选用人食管癌细胞(esophageal cancer cells,ECCs)ECA-109.设计分为4组:空白对照组、顺铂组、单纯加钼组、顺铂加钼组,后3组均采用不同的浓度进行试验.用MTT法检测各组对人食管癌细胞ECA-109的生长抑制作用;流式细胞仪检测各组p75NTR百分率的变化.结果:顺铂组各浓度对食管癌细胞ECA-109有一定的抑制作用,且对食管癌干细胞也有不同程度的抑制作用,并且随着给药浓度和时间的增加均呈增强趋势;单纯加钼组对食管癌细胞ECA-109和对食管癌干细胞的抑制作用均不明显;顺铂加钼组对食管癌细胞ECA-109和食管癌干细胞的抑制作用则明显增强,与单用同浓度顺铂组及空白对照组比较有差异性(P<0.05),且呈一定的浓度、时间依赖性.结论:钼可明显增强顺铂对食管癌细胞ECA-109和食管癌干细胞的抑制作用,而单用钼则达不到理想的效果,说明钼可作为化疗增敏剂,为其作为食管癌化疗的辅助剂提供了实验依据.

NGF及其受体trkA及p75NTR在子宫内膜异位症患者在位内膜中的表达及其与内异症疼痛的关系

目的:研究子宫内膜异位症(内异症)患者在位内膜神经生长因子(NGF)及其受体trkA、p75NTR的表达,探讨上述因子与内异症疼痛的关系。方法:选择就诊于北京协和医院并进行了腹腔镜手术的28例子宫内膜异位症患者作为研究组,非子宫内膜异位症患者10例作为对照组(B组),收集上述患者分泌期在位子宫内膜。根据患者有无痛经,分为内异症疼痛组(A1组,18例)及内异症非疼痛组(A2组,10例)。采用免疫组化比较各组病灶中NGF及其受体trkA、p75NTR的表达,并分析其与痛经的关系。结果:各组在位内膜腺上皮中NGF的表达显著高于间质(P<0.05);内异症疼痛组腺上皮NGF表达较非疼痛组明显升高(359.9±18.7 vs 201.3±34.3,P<0.05)。p75NTR主要在子宫内膜间质细胞中表达;内异症组明显高于非内异症组(58.8±21.1、22.5±16.1 vs 0,P<0.05);内异症疼痛组较非疼痛组p75NTR表达明显升高(58.8±21.1 vs 22.5±16.1,P<0.05)。trkA在非内异症组子宫内膜间质中表达明显高于腺上皮(P<0.05);在内异症组腺上皮中,trkA的表达较非内异症组明显增高(P<0.05);trkA的表达量与内异症患者疼痛无关。结论:p75NTR可能参与内异症的发病,NGF及其受体p75NTR在在位内膜中的表达与患者疼痛相关,表明其可能参与了内异症疼痛发病机制。

脑白质损伤新生大鼠脑白质P75NTR蛋白与RhoA mRNA的表达及意义

目的最近研究发现NgR-P75NTR-RhoA信号通路在神经损伤和重塑方面发挥关键作用,但其确切传导机制及在缺氧缺血后新生动物P75NTR对下游分子RhoA调控变化尚不清楚。该实验在建立新生大鼠缺氧缺血性脑白质损伤(WMD)模型基础上,观察WMD新生大鼠脑白质P75NTR和RhoA mRNA表达变化,探讨WMD时两者的关系及意义,为临床治疗早产儿WMD提供新思路和实验依据。方法制备新生大鼠WMD模型,光镜及电镜观察脑组织形态学改变。应用免疫组织化学方法及荧光定量RT-PCR检测对照组及WMD12,24,48,72h和7d组病变侧脑白质P75NTR蛋白及RhoA mRNA表达变化。结果光镜和电镜形态学发现WMD组缺氧缺血48h后即有显著的脑室周围脑白质损伤。WMD组大鼠纹状体和胼胝体P75NTR蛋白水平12h开始升高,48h达峰值,至72h略有下降,与对照组比较差异有显著性,均P<0.01,之后下降明显,第7天与对照组比较差异无统计学意义(P>0.05)。WMD组大鼠脑白质RhoA mRNA表达12h开始升高,48h达到峰值,与对照组比较,差异有显著性,均P<0.05。72h仍高于对照组水平,之后开始下降,第7天与对照组比较差异无显著性(P>0.05)。结论WMD新生大鼠脑白质中P75NTR蛋白水平呈现先上升后下降的趋势。其升高与介导神经细胞凋亡和抑制神经轴突再生可能有关,表达下降则与缺氧缺血性损伤加重神经细胞坏死相关。RhoA mRNA的表达变化趋势与P75NTR一致,提示P75NTR水平升高可促使RhoA mRNA高表达。

p75^(NTR)在乳腺癌中的表达及其临床意义

目的:探讨神经营养因子受体p75NTR在乳腺癌中的表达及与临床病理、激素受体、分子分型之间是否存在相关性。方法:利用免疫组织化学法检测186例乳腺癌组织p75NTR、ER、PR、HER2、Ki-67的表达情况,分析p75NTR与临床病理参数间的相关性。结果:p75NTR在乳腺癌组织中阳性表达占11.3%(21/186),p75NTR的表达与组织分级、Ki-67蛋白水平正相关(P<0.05),与ER表达负相关(P<0.05),与肿瘤大小、是否绝经、淋巴结转移等无关(P>0.05),但在淋巴结转移分层分析中淋巴结转移<4枚与淋巴结≥4之间,p75NTR的表达与之相关(P<0.05);p75NTR表达与Luminal B型及三阴乳腺癌亚型显著相关。结论 :p75NTR可预测三阴乳腺癌及Luminal B亚型,较准确地进行分子分型,为指导临床分层治疗提供依据。

前列腺癌神经生长因子受体TrkA/p75NTR比值与临床分期、分级的关系

目的：探讨神经生长因子（NGF）的两种受体（TrkA和p75NTR）在前列腺癌（PCa）发生、发展中的表达规律及作用机制。方法：采用免疫组化法研究62例PCa和35例良性前列腺增生（BPH）组织中TrkA及p75NTR蛋白的表达，并结合临床资料进行统计分析。结果：通过成组t检验，发现自BPH组织至低分化PCa组织（Gleason 8～10分），随着组织分化逐渐降低或临床分期逐渐增高，TrkA受体表达显著增强，p75NTR受体表达显著减低，TrkA／p75NTR比例显著增大。在BPH组织中两者比例为0．32，在Gleason评分6分的PCa组织中为0．52，在7分的组织中为1．65，而在8～10分的组织中为5．75；在pT2期组织中两者比例为0．89，在pT3a期为1．5，在pT3b期为3．75，在有淋巴结转移（pTxN1）的组织中为7．00。结论：TrkA／p75NTR比例的失调性增高，可能是前列腺细胞恶变后的基本特征之一。TrkA／p75NTR比值越高，组织分化程度越低，临床分级、分期越高，患者预后可能越差。

神经营养因子受体p75NTR在乳腺癌耐药细胞中的表达及其与多药耐药的相关性

目的:探讨神经营养因子受体p75NTR在乳腺癌耐药细胞中的表达及其与多药耐药的相关性。方法:Western blot检测多种乳腺癌细胞系中p75NTR蛋白表达;基因重组构建p75NTR的正义及反义载体并检测转染p75NTR及p75NTR-si RNA后乳腺癌耐药细胞系MDA-MB-231/ADR中p75NTR蛋白表达;CCK-8法检测MDA-MB-231/ADR对各种化疗药物的敏感性及转染p75NTR及p75NTR-si RNA后对耐药的影响。结果:p75NTR在乳腺癌耐药细胞系中的表达高于亲本细胞;p75NTR过表达载体上调MDA-MB-231/ADR中p75NTR的表达;过表达p75NTR可增强MDA-MB-231/ADR对ADM、GEM和OXA的耐药性。结论:p75NTR在乳腺癌耐药细胞系中的表达高于其亲本细胞,过表达p75NTR能够降低多药耐药细胞对化疗药物的敏感性而促进其多药耐药性。

丙泊酚对原代培养大鼠皮层神经元BDNF和p75NTR水平的影响

目的探讨丙泊酚对原代培养大鼠皮层神经元凋亡的影响及可能机制。方法原代培养7 d的大鼠皮层神经元,随机分为两组:溶剂对照组(给予相同容积的20%脂肪乳剂),丙泊酚组(丙泊酚终浓度为500μmol/L),上述药物处理皮层神经元12 h后,用光学显微镜观察两组皮层神经元的形态学变化,MTT法检测神经元存活率的变化,Western blot法检测神经元脑源性神经营养因子(BDNF)、p75神经营养因子受体(p75NTR)以及B淋巴细胞瘤-2基因(Bcl-2)蛋白水平的变化。结果与溶剂对照组比较,丙泊酚组光镜下观察显示皮层神经元数量明显减少,胞体立体感消失,细胞轮廓不清,神经元轴突断裂。神经元存活率显著性下降(P<0.01),BDNF和Bcl-2蛋白水平显著性下降(P<0.01),p75NTR蛋白水平显著性增加(P<0.01)。结论丙泊酚可引起发育期原代培养皮层神经元损伤,其机制可能与下调BDNF、Bcl-2和上调p75NTR蛋白水平有关。

p75NTR对舌鳞癌Tca8113细胞凋亡的影响

目的:探讨p75NTR基因对舌鳞癌Tca8113细胞凋亡的影响。方法:流式细胞技术分选Tca8113细胞系中p75NTR阳性细胞及阴性细胞,对阳性细胞用脂质体瞬时转染荧光标记的p75NTR siRAN,实时定量RT-PCR检测p75NTR基因,western blot检测p75NTR蛋白表达;流式细胞仪Annexin V/PI双染色标记法进行凋亡检侧;MTT检测细胞增殖的影响。结果:p75NTR表达阳性的Tca8113细胞经p75NTR siRNA转染后p75TNR的表达被抑制;细胞凋亡率明显增加(P<0.05),细胞增殖率明显降低。结论:p75NTR在Tca8113细胞凋亡中具有调控作用。

p75^(NTR)阳性人食管鳞癌细胞的干细胞特性研究

目的探讨p75NTR阳性人食管鳞癌细胞的干细胞特性。方法取15例新鲜人食管鳞癌组织制成单细胞悬液,分别获取p75NTR阳性和p75NTR阴性细胞,进行Transwell侵袭试验、耐化疗药物试验及裸鼠成瘤试验。结果15例新鲜人食管鳞癌组织中有7例发现p75NTR表达,其阳性表达率最高为10.37%,p75NTR阳性和p75NTR阴性细胞在侵袭性、对化疗药物的耐受能力及致瘤能力上差异有统计学意义。结论 p75NTR阳性较p75NTR阴性食管鳞癌细胞具有更强的侵袭性、耐化疗能力及致瘤能力,可能富集人食管鳞癌干细胞。

蛴螬对激光损伤兔血-视网膜屏障后视网膜TekA、p75NTR表达的影响

目的:探讨蛴螬促进激光损伤兔血-视网膜屏障后的修复作用及机理。方法:30只成年健康有色家兔随机分为正常对照组、模型对照组、蛴螬组。采用激光损伤血-视网膜屏障动物模型,在屏障损伤后1周及2周2个时相,观察蛴螬对兔血-视网膜屏障损伤修复情况、血-视网膜屏障组织形态结构及神经营养因子受体TrkA、p75NTR表达及影响。结果:蛴螬能促进损伤的血-视网膜屏障修复,减轻激光导致的视网膜组织及细胞形态学损伤,促进TrkA、p75NTR的表达,抑制视网膜细胞增殖与变性,从而改善视网膜功能。结论:蛴螬可能通过改善视网膜组织能量代谢,清除氧自由基,促进神经营养因子受体的表达,抑制视细胞增殖,从而起到保护血-视网膜屏障组织结构,促进损伤后功能恢复的作用。

消异方对子宫内膜异位症模型大鼠异位内膜P75NTR的影响

目的:观察消异方对子宫内膜异位症大鼠异位内膜P75NTR的影响,探讨消异方治疗子宫内膜异位症的机制。方法:采用自体手术移植法建立大鼠子宫内膜异位症模型,随机分为模型组、米非司酮组、散结镇痛胶囊组、消异方低、中、高剂量组。造模成功各组给药4W,免疫组化方法检测大鼠异位子宫内膜组织P75NTR的表达情况。结果:模型组异位内膜中P75的表达水平明显高于米菲司酮组、散结镇痛胶囊组和中药消异方各剂量组(P<0.05)。结论:消异方能降低大鼠子宫内膜P75NTR的含量,以达到治疗子宫内膜异位症所引起的慢性盆腔疼痛的作用。