Effect of electro-acupuncture on substance P, its receptor and corticotropin-releasing hormone in rats with irritable bowel syndrome

AIM： To investigate the effect and mechanism of electro-acupuncture lEA） at ST25 and ST37 on irritable bowel syndrome （IBS） of rats. METHODS： A total of 21 male Sprague-Dawley rats were randomly divided into normal group, model group and EA group. A rat model of IBS was established by constraining the limbs and distending the colorectum of rats. Rats in EA group received bilateral EA at ST25 and ST37 with a sparse and intense waveform at a frequency of 2/50 Hz for 15 min, once a day for 7 d as a course. Rats in normal and model groups were stimulated by distending colorectum （CR）. An abdominal withdrawal reflex （AWR） scoring system was used to evaluate improvements in visceral hypersensitivity. Toluidine blue-improved method, immunohistochemistry and radioimmunoassay were used to observe mucosal mast cells （MC）, changes of substance P （SP） and substance P receptor （SPR） in colon and change of corticotropin-releasing hormone （CRH） in hypothalamus. RESULTS： The threshold of visceral sense was significantly lower in model group than in normal group,and significantly higher in EA group than in model group. The number of mucosal MC was greater in model group than in normal group and significantly smaller in EA group than in model group. The CRH level in hypothalamus of rats was significantly higher in model group than in normal group, which was remarkably decreased after electro-acupuncture treatment. The SP and SPR expression in colon of rats in model group was decreased after electro-acupuncture treatment. CONCLUSION： EA at ST25 and ST37 can decrease the number of mucosal MC and down-regulate the expression of CRH in hypothalamus, and the expression of SP and SPR in colon of rats with IBS.

Effects of electroacupuncture on corticotropin-releasing hormone in rats with chronic visceral hypersensitivity

AIM: To investigate the effect of electroacupuncture on corticotropin-releasing hormone(CRH) in the colon, spinal cord, and hypothalamus of rats with chronic visceral hypersensitivity.METHODS: A rat model of chronic visceral hypersensitivity was generated according to the internationally accepted method of colorectal balloon dilatation. In the 7th week after the procedure, rats were randomly divided into a model group(MG), electroacupuncture group(EA), and sham electroacupuncture group(S-EA). After treatment, the abdominal withdrawal reflex(AWR) score was used to assess the behavioral response of visceral hyperalgesia. Immunohistochemistry(En Vision method), ELISA, and fluorescence quantitative PCR methods were applied to detect the expression of CRH protein and m RNA in the colon, spinal cord, and hypothalamus.RESULTS: The sensitivity of the rats to the colorectal distension stimulus applied at different strengths(20-80 mm Hg) increased with increasing stimulus strength, resulting in increasing AWR scores in each group. Compared with NG, the AWR score of MG was significantly increased(P < 0.01). After conducting EA, the AWR scores of the rats were decreased compared with MG rats. The relative expression of CRH m RNA in the colon, spinal cord, and hypothalamus of MG rats was significantly increased compared with NG rats(P < 0.01). CRH m RNA in the colon and spinal cord of EA and S-EA rats was decreased to varying degrees(P > 0.05) compared with normal rats(NG). However, the decrease in EA compared with MG rats was statistically significant(P < 0.01). The average optical density of CRH expression in the colon of the MG rats was significantly enhanced compared with NG(P < 0.05), while the average optical density of CRH expression in the EA and S-EA rats was significantly decreased compared with MG rats(P < 0.01, P < 0.05, respectively). Compared with MG rats, the CRH concentration in the spinal cord of EA rats was significantly reduced(P < 0.01), but there was no significant change in S-EA rats(P > 0.05).CONCLUSION: Electroacupuncture at the Shangjuxu acupoint was able to significantly reduce the visceral hypersensitivity in rats, and regulated the expression of CRH protein and m RNA in the colon, spinal cord and hypothalamus at different levels, playing a therapeutic role in this model of irritable bowel syndrome.

Follicular Fluid Cortisol Releasing Hormone (CRH) Levels and Assisted Reproductive Treatment (ART) Outcomes

Purpose: Can Cortisol Releasing Hormone (CRH) levels in follicular fluid predict outcomes following assisted reproductive treatment (ART) cycles? Methods: Prospective cohort study of 50 women undergoing in vitro fertilisation (IVF)/intra-cytoplasmic sperm injection (ICSI) cycles over a two month study period. All patients were treated on the long stimulation protocol;follicular fluid was aspirated and pooled for each patient. The samples were processed appropriately and assayed using CRH radioimmunoassay (RIA). Results: This study confirmed that CRH was present in follicular fluid. The average level detected was 173 ± 9 pg/mL (mean ± standard error of mean [SEM]). The data suggests a positive correlation of CRH follicular fluid levels greater than 145 pg/mL with successful ART outcomes. Conclusion: The data indicates a positive correlation between ART outcomes and the presence of follicular fluid CRH levels greater than 145 pg/mL. The results should be interpreted with caution due to the small sample size and pooling of follicular fluid per patient. Furthermore, the pooling of follicular fluid is not representative of CRH levels in an individual follicle, and thus, mature oocyte. This study serves as a reminder to what has previously been hypothesised.

Neuroimmune connections between corticotropinreleasing hormone and mast cells:novel strategies for the treatment of neurodegenerative diseases

Corticotropin-releasing hormone is a critical component of the hypothalamic–pituitary–adrenal axis,which plays a major role in the body’s immune response to stress.Mast cells are both sensors and effectors in the interaction between the nervous and immune systems.As first responders to stress,mast cells can initiate,amplify and prolong neuroimmune responses upon activation.Corticotropin-releasing hormone plays a pivotal role in triggering stress responses and related diseases by acting on its receptors in mast cells.Corticotropin-releasing hormone can stimulate mast cell activation,influence the activation of immune cells by peripheral nerves and modulate neuroimmune interactions.The latest evidence shows that the release of corticotropin-releasing hormone induces the degranulation of mast cells under stress conditions,leading to disruption of the bloodbrain barrier,which plays an important role in neurological diseases,such as Alzheimer’s disease,Parkinson’s disease,multiple sclerosis,autism spectrum disorder and amyotrophic lateral sclerosis.Recent studies suggest that stress increases intestinal permeability and disrupts the blood-brain barrier through corticotropin-releasing hormone-mediated activation of mast cells,providing new insight into the complex interplay between the brain and gastrointestinal tract.The neuroimmune target of mast cells is the site at which the corticotropin-releasing hormone directly participates in the inflammatory responses of nerve terminals.In this review,we focus on the neuroimmune connections between corticotropin-releasing hormone and mast cells,with the aim of providing novel potential therapeutic targets for inflammatory,autoimmune and nervous system diseases.

Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress

Objective Corticotropin-releasing hormone（CRH）plays an important role in neuroendocrine,autonomic and behavioral responses to stressors.In the present study,the effect of chronic unpredictable mild stress（CUMS）on CRH neurons was investigated in rat brain.Methods The rats were exposed to one of the stressors each day for 21 d.Immunostaining was performed to detect the CRH-positive neurons in the paraventricular nucleus（PVN）of the hypothalamus and in amygdala.Results After the stress protocol,the animals showed a reduction in body weight gain as well as reduced sucrose preference and locomotor activity.Interestingly,the CRH neurons in both PVN and central nucleus of the amygdala（CeA）were stimulated by CUMS.The densities of CRH-containing neurons in both PVN and CeA were significantly higher than those in control group.Conclusion The CRH systems in PVN and CeA may both contribute to depression-like behaviors during CUMS.

电针对佐剂性关节炎大鼠病灶局部CRH阳性细胞免疫反应性的影响

目的研究电针对佐剂性关节炎大鼠的镇痛作用机制是否与其对病灶局部CRH阳性细胞免疫反应性的影响有关。方法本课题采用佐剂性关节炎模型大鼠,研究电针同侧环跳穴、阳陵泉穴对运动障碍的改善作用,采用免疫组化技术,观察电针对致炎后模型大鼠外踝关节周围皮肤及皮下组织CRH阳性细胞免疫反应性的影响,同时针刺非穴位和对侧穴位进行对照,探讨针刺作用的穴位特异性。结果造模后,除空白组外其他各组大鼠运动障碍明显,分别电针同侧及对侧穴位可显著改善炎症大鼠的运动障碍。炎症组病灶局部CRH阳性细胞的面积百分比、平均光密度均显著高于空白对照组,电针同侧穴位、对侧穴位显著降低炎症组CRH阳性细胞的平均光密度,而非经穴电针对照组没有显著疗效。结论电针同侧穴位、对侧穴位可通过促使定向迁移至炎性痛病灶的免疫细胞合成并释放CRH,从而发挥镇痛作用,与中医“巨刺法”的说法相呼应。

海上150m氦氧饱和-182m巡回潜水对潜水员血浆和尿液CRH、β-EP含量的影响

目的 :探讨海上大深度饱和潜水对潜水员血浆和尿液中CRH、β EP含量的影响。 方法 :用放射免疫法检测潜水员饱和前后血浆CRH、β EP含量和潜水员在饱和潜水前、加压后、饱和暴露期间及减压后尿中CRH和 β EP的含量。 结果 :血浆CRH含量在饱和潜水后显著高于饱和潜水前 (P <0 .0 1 )。尿液中的CRH、β EP含量在加压后、饱和期间及减压后均显著高于饱和潜水前 (P <0 .0 5)。结论 :大深度饱和潜水能引起潜水员血浆和尿液中CRH、β EP含量的改变 ,CRH、β

肠吉泰对腹泻型肠易激综合征大鼠CRH、SPmRNA表达的影响

目的观察肠吉泰对腹泻型肠易激综合征肝郁脾虚证模型大鼠促肾上腺皮质激素释放激素(CRH)、P物质(SP)mRNA表达的影响,探讨其治疗机制。方法将60只雄性SD大鼠随机分为正常组,模型组,肠吉泰低、中、高剂量组和匹维溴铵(得舒特)组。除正常组外,各组大鼠予束缚应激加大黄泻下及结直肠扩张法复制模型,并予以相应药物治疗。大鼠处死后剖取小肠,测量小肠墨汁推进率;取下丘脑及结肠标本用RT-PCR半定量检测CRH mRNA及SP mRNA的表达。结果与正常组比较,各组造模大鼠的下丘脑CRH、SPmRNA表达均升高,差异有统计学意义(P<0.05);与模型组比较,除肠吉泰低剂量组大鼠下丘脑的SP mRNA表达差异无统计学意义外(P>0.05),其余各治疗组大鼠CRH、SPmRNA表达下调(P<0.05,P<0.01);与得舒特组比较,肠吉泰高、中剂量组大鼠结肠SP mRNA降低,差异有统计学意义(P<0.05,P<0.01)。与模型组比较,各治疗组大鼠的大便频次显著降低、大便性状明显改善(P<0.05),小肠推进率降低(P<0.05),且肠吉泰与得舒特组大鼠大便频次、大便性状及小肠墨汁推进率差异无统计学意义(P>0.05)。结论肠吉泰对于腹泻型肠易激综合征肝郁脾虚证模型大鼠具有改善应激状态、调节肠动力、解除内脏高敏感性等治疗作用。推测肠吉泰通过调节大鼠下丘脑CRH、SP mRNA表达及结肠SP mRNA表达,改善腹泻型肠易激综合征肝郁脾虚证模型大鼠对束缚应激反应导致肠动力的紊乱,改善内脏痛觉敏感状态。

CRH对人子宫平滑肌细胞Cx43磷酸化水平及细胞间隙连接通讯的影响

目的:探讨人类促肾上腺皮质激素释放激素(CRH)对人子宫平滑肌细胞间隙连接蛋白43磷酸化水平(P-Cx43)以及其对子宫平滑肌细胞间隙连接通道(GJIC)功能的影响。方法:原代培养人未孕子宫平滑肌细胞,给予不同浓度的CRH(0,5.85,58.5,585,5850 pmol/L)进行干预,采用Western印迹分别定量检测CRH各浓度组中子宫平滑肌细胞P-Cx43与非磷酸化Cx43蛋白(NP-Cx43)的表达;细胞划痕实验检测CRH各浓度组中GJIC的变化。结果:CRH各干预组子宫平滑肌细胞中P-Cx43蛋白的表达明显高于对照组,随着CRH干预浓度的递增,呈剂量依赖趋势,各组之间差异有统计学意义(P<0.01);而对照组和干预组之间NP-Cx43蛋白的表达差异无统计学意义(P>0.05);CRH干预后各浓度组荧光黄染料在子宫平滑肌细胞中传输的细胞数明显高于对照组,各组之间比较差异有统计学意义(P<0.01)。同时,随着CRH干预浓度的递增,荧光黄染料传输至最远细胞级所需要的时间呈剂量依赖趋势,各组之间比较差异有统计学意义(P<0.01)。结论:CRH可上调原代子宫平滑肌细胞中P-Cx43蛋白的表达,增强GJIC的功能。

母血中游离CRH、PLAC1、Selectin-P的mRNA表达水平与子痫前期的相关性研究

目的:比较孕妇血浆中胎盘来源的外周血促肾上腺皮质激素释放激素(CRH)、胎盘特异蛋白-1(PLAC1)、选择素P(Selectin-P)基因的mRNA表达水平在子痫前期患者和正常孕妇之间的区别。方法:选择30例子痫前期病例(病例组)及40例正常孕妇(对照组)采集外周血提取RNA,分析上述3个基因的游离mRNA表达水平,并在两组间采用t检验比较。结果:CRH、PLAC1和Selectin-P在病例组及对照组的孕妇外周血中均有表达,病例组孕妇外周血中CRH、PLAC1、Selectin-P的表达水平明显高于对照组(P<0.05)。结论:孕母血浆中的胎盘来源的游离CRH、PLAC1、Selectin-P表达水平对于妊娠期高血压疾病,子痫前期的发病具有预测价值。

黄斑蓝子鱼CRH基因的克隆及其在浅水应激后的mRNA表达

鱼类应激时主要启动两种生理反应系统,即"交感-嗜铬组织"系统/和/或"下丘脑-垂体-肾间组织轴"(HPI轴)系统.在实际生产操作中,鱼类容易受到浅水暴露应激.为了探讨黄斑蓝子鱼在受到浅水应激后HPI轴是否被激活,本研究克隆了下丘脑中启动HPI轴活性的关键因子—促肾上腺皮质激素释放激素(CRH)的基因,并检测其在应激前和受到浅水应激后不同时间点(0、20、40、60、80 min)的mRNA水平.结果显示,CRH前体的cDNA全长为1025 bp,编码170个氨基酸(aa),分别由一个信号肽(24个aa)、一个功能未知保守区(13个aa)和一个成熟肽(41个aa)组成;该CRH前体和成熟肽与其他鱼类的相应肽分别具有62%-98%和78%-100%的序列相似性.当鱼体受到短暂(4 min)浅水应激后80 min内,脑中CRH mRNA水平在应激前后无显著变化(P>0.05),说明黄斑蓝子鱼在受到急性浅水应激后可能主要启动"交感-嗜铬组织"系统而不是HPI轴.

两类促肾上腺皮质释放激素（CRH）拮抗剂的分子场分析

采用比较分子相似性指数分析方法(CoMSIA)及比较分子场分析方法(CoMFA)研究了两组CRH拮抗剂结构与活性的关系.在两种方法中,都考虑了静电场、立体场以及氢键场对构效关系的影响,结果表明采用CoMSIA得到构效关系模型要明显优于采用CoMFA得到的构效关系模型.在CoMSIA计算中,当引入疏水场时,三维构效关系模型能得到明显的改善,通过这个三维构效关系模型,可以较为精确地预测化合物的活性.通过分析分子场等值面图在空间的分布,可以观察到叠合分子周围的立体、静电以及疏水特征对化合物活性的影响.

四磨汤对功能性排便障碍模型大鼠CRH、脑肠肽SP、及肥大细胞的干预作用

目的探讨功能性排便障碍(functional constipationnal disorder FC)发病的可能机制,并尝试解释中药四磨汤治疗功能性排便障碍的作用途径。方法 110只小鼠被随机分为6组:正常对照组,西药组,模型组,中药低剂量组,中药中剂量组,中药高剂量组。治疗2周后,测定各组大鼠的下丘脑部、脑干部位的肾上腺皮质激素释放因子(Corticotropin-releasing hormone,CRH)水平、脊髓腰段的P物质(substance P,SP)含量,采用免疫组化法观察肠粘膜肥大细胞活化状态(c-fos基因表达情况)及中药四磨汤对其影响。结果功能性排便障碍模型大鼠经四磨汤灌胃治疗2周后,与未用药的模型组相比,大鼠内脏的敏感性明显降低(P<0.05)。与正常组相比,功能性排便障碍模型组大鼠脑干部、下丘脑部位的CRH水平明显升高,大鼠脊髓腰段的SP含量降低,肠粘膜c-fos基因表达总阳性显色细胞数总数降低,两组比较P<0.05,差异具有统计学意义;与模型组相比,中药高、中、低剂量组、西药组大鼠脑干部、下丘脑的CRH水平均有所降低,大鼠脊髓腰段的SP含量升高,肠粘膜c-fos基因表达总阳性显色细胞数升高,两组间比较P<0.05,差异具有统计学意义。结论功能性排便障碍模型大鼠脑干、下丘脑CRH含量、脊髓P物质表达的改变提示与功能性排便障碍的发病相关。中药四磨汤能降低功能性排便障碍模型大鼠脑干、下丘脑CRH含量、升高脊髓P物质含量与c-fos基因表达水平,其作用机制可能是与影响脑肠轴通路有关。

CRH及其受体-1在分娩发动中的作用

目的比较早产及足月分娩剖宫产产妇血清肾上腺皮质激素释放激素(CRH)水平及子宫下段中促肾上腺皮质激素释放激素受体-1(CRH-R1)的表达情况,分析其在分娩发动中的作用。方法按难免早产、足月分娩发动、足月分娩未发动分为3组,术前测定血清中CRH水平,于剖宫产中取子宫下段平滑肌,用免疫组化的方法检测CRH-R1在子宫下段的表达。结果3组间CRH水平差异无统计学意义(P>0.05),均为孕期较高水平。难免早产组、足月分娩发动组CRH-R1在子宫下段肌层中呈高表达状,其表达指数明显高于足月分娩未发动组(t值分别为5.000、6.295,均P<0.05)。难免早产组、足月分娩发动组CRHR1在子宫下段肌层中的表达差异无统计学意义(P>0.05)。结论 CRH为参与人类分娩启动因子之一。母体血浆CRH水平有望作为早产预测和预后指标,其作用的发挥还有赖于子宫体中CRH-R1的表达。

妊娠期血浆CRH、E_2及P与早产关系的研究

目的：探讨促肾上腺激素释放激素（corticotropin releasing hormone, CRH）、雌二醇（estradiol, E2）及孕激素（progesterone, P）在妊娠期间的浓度变化及其在早产中的预测作用。方法选取正常妊娠组孕妇54例,先兆早产组孕妇54例,采集外周静脉血分离血浆,用免疫化学发光法测定E2、P,放射免疫法测定CRH水平。结果①正常妊娠血CRH均值28～33周组与＆gt;37周组比,明显低于＆gt;37周组,经t检验P〈0.05；血E2各组间均值经t检验P〉0.05,差异无统计学意义；血P各组均值,28～33周组明显高于＆gt;37周组,经t检验P〈0.05,差异有统计学意义,其余各组差异无统计学意义。②正常妊娠组和先兆早产组在妊娠28～33周血CRH分别为（68.23＆#177;13.34）ng/L和（298.42＆#177;162.78）ng/L；在34～36周分别为（132.75＆#177;126.3） ng/L和（354.42＆#177;50.46） ng/L,经t检验, P值均＆lt;0.05,差异有统计学意义。正常妊娠组和先兆早产组血E2在28～33周分别为（128.72＆#177;50.83）μg/L和（152.94＆#177;31.7）μg/L；在34～36周分别为（136.24＆#177;62.41）μg/L和（173.58＆#177;92.3）μg/L,两组均值经t检验, P值均＆lt;0.05,差异无统计学意义。正常妊娠组和先兆早产组血P在28～33周分别为（523.52＆#177;105.43）μg/L和（353.21＆#177;52.21）μg/L,34～36周（483.24＆#177;113.52）μg/L和（310.25＆#177;83.02）μg/L,差异有统计学意义。结论血P在妊娠晚期各孕周组间变化较为明显,妊娠＆gt;37周之后明显下降。妊娠晚期正常妊娠组中的血浆CRH值随着孕周增加而逐渐升高,而血E2值无明显变化。

E_2、P、CRH在早产发病中的作用

目的观察妊娠晚期孕妇外周血中雌二醇(E2)、孕酮(P)、促肾上腺皮质激素释放激素(corticotropin-releasing hormone,CRH)的变化及其在早产发病中的作用和它们之间的相互关系.方法选取正常妊娠组孕妇60例,先兆早产组孕妇63例(早产组21例,继续妊娠组42例),采集外周静脉血分离血浆,用免疫化学发光法测定E2、P,放射免疫法测定CRH水平.结果1)妊娠晚期正常孕妇血中的CRH质量浓度随着孕周增加而逐渐升高,而血E2质量浓度无明显变化,P质量浓度31～32周达到高峰,之后明显下降.2)正常妊娠组和先兆早产组各孕周组间血CRH、P比较差异均有统计学意义(P＜0.01),而正常妊娠组和先兆早产组妊娠29～30周和31～32周2个孕周组间血E2比较差异无统计学意义(P＞0.05),妊娠33～34周和35～36周2孕周组间比较差异有统计学意义(分别为P＜0.01和P＜0.05).3)早产组CRH、E2显著高于继续妊娠组,差异有统计学意义(P＜0.01).早产组P显著低于继续妊娠组,差异有统计学意义(P＜0.05).结论1)CRH可能是分娩发动的重要因素.2)CRH在早产发病中起重要作用,CRH的异常升高可能决定了分娩时间的提前.监测孕妇血CRH的变化有望成为预测早产的可靠指标.3)与E2相比,P在早产发动中发挥更重要的作用.

褐牙鲆早期发育阶段CRH基因表达及受甲状腺激素的影响

【目的】探析褐牙鲆仔鱼早期发育阶段促肾上腺皮质激素释放激素基因(CRH)的表达情况及受甲状腺激素的影响作用,为开展牙鲆的人工繁育提供科学依据。【方法】通过实时荧光定量PCR检测褐牙鲆早期发育阶段CRH基因表达量,以ELISA测定褐牙鲆仔鱼甲状腺激素(T3和T4)水平,并测定经外源T3浸泡处理后早期发育褐牙鲆仔鱼CRH基因表达量的变化情况,探究CRH和甲状腺激素在褐牙鲆早期发育阶段的影响及作用关系。【结果】1~8日龄褐牙鲆仔鱼CRH基因相对表达量呈先升高后降低的变化趋势,在5日龄达最高值,显著高于其他日龄的仔鱼(P<0.05,下同)。10~42日龄褐牙鲆仔鱼CRH基因主要在其头部表达,尾部CRH基因的相对表达量随着生长发育的进程而逐渐增加。褐牙鲆仔鱼变态前期甲状腺激素T4含量逐渐增加,变态高峰期迅速升高,在变态后期呈下降趋势。较其他早期发育时期,甲状腺激素T3在褐牙鲆变态期维持高水平,但含量低于甲状腺激素T4。22日龄褐牙鲆仔鱼经50 nmol/L外源T3处理2 h后,其头部和尾部CRH基因的相对表达量显著升高;但以外源T3处理8 h后,无论是头部还是尾部,CRH基因的相对表达量均呈显著下降趋势。【结论】褐牙鲆早期变态发育需CRH基因高表达及甲状腺激素积累,二者对褐牙鲆早期变态发育阶段具有重要作用并呈互相代偿效应。

Mucosa repair mechanisms of Tong-Xie-Yao-Fang mediated by CRH-R2 in murine,dextran sulfate sodium-induced colitis

AIM To explore the significance of corticotropin-releasing hormone(CRH)-receptor(R)2 in mucosal healing of dextran sulfate sodium(DSS)-induced colitis and the effect of Tong-Xie-Yao-Fang(TXYF) on CRH-R2 expression and regulation.METHODS Ulcerative colitis was induced in mice by administration of 3%(w/v) DSS for 7 d. Once the model was established,mice were administered urocortin-2(30 μg/kg), a peptide which binds exclusively to CRH-R2, or various doses of aqueous TXYF extracts(2.8-11.2 g/kg), a CRH-R2 antagonist Astressin(Ast)2B(20 μg/kg), Ast2B + Ucn2, or Ast2B with various doses of aqueous TXYF extracts for 9 d. Colonic mucosal permeability was then evaluated by measuring the fluorescence intensity in serum. The colitis disease activity index(DAI), histology, body weight loss and colon length were assessed to evaluate the condition of colitis. Terminal deoxynucleotidyl transferase d UTP nick-end labeling was used to detect apoptosis of the intestinal epithelial cells. The expression level of Ki-67 represented the proliferation of colonic epithelial cells and was detected by immunohistochemistry. The expression levels of inflammation cytokines IL-6, TNF-α and CXCL-1 were examined in colon tissues using real-time PCR and ELISA kits.RESULTS Compared with the DSS group, mice treated with the CRH-R2 antagonist Ast2B showed greater loss of body weight, shorter colon lengths(4.90 ± 0.32 vs 6.21 ± 0.34 cm, P < 0.05), and higher DAI(3.61 ± 0.53 vs 2.42 ± 0.32, P < 0.05) and histological scores(11.50 ± 1.05 vs 8.33 ± 1.03, P < 0.05). Additionally, the Ast2B group showed increased intestinal permeability(2.76 ± 0.11 μg/mL vs 1.47 ± 0.11 μg/mL, P < 0.001), improved secretion of inflammatory cytokines in colon tissue, and reduced colonic epithelial cell proliferation(4.97 ± 4.25 vs 22.51 ± 8.22, P < 0.05). Increased apoptosis(1422.39 ± 90.71 vs 983.01 ± 98.17, P < 0.001) was also demonstrated. The Ucn2 group demonstrated lower DAI(0.87 ± 0.55 vs 2.42 ± 0.32, P < 0.001) and histological scores(4.33 ± 1.50 vs 8.33 ± 1.03, P < 0.05). Diminished weight loss, longer colon length(9.58 ± 0.62 vs 6.21 ± 0.34 cm, P < 0.001), reduced intestinal permeability(0.75 ± 0.07 vs 1.47 ± 0.11 μg/mL, P < 0.001), inhibited secretion of inflammatory cytokines in colon tissue and increased colonic epithelial cell proliferation(90.04 ± 15.50 vs 22.51 ± 8.22, P < 0.01) were all observed. Reduced apoptosis(149.55 ± 21.68 vs 983.01 ± 98.17, P < 0.05) was also observed. However, significant statistical differences in the results of the Ast2 B group and Ast2 B + Ucn2 group were observed. TXYF was also found to ameliorate symptoms of DSS-induced colitis in mice and to promote mucosal repair like Ucn2. There were significant differences between the Ast2B + TXYF groups and the TXYF groups.CONCLUSION CRH-R2 activates the intestinal mucosal antiinflammatory response by regulating migration, proliferation and apoptosis of intestinal epithelial cells in colitisinduced mice, and plays an important antiinflammatory role. TXYF promotes mucosal repair in colitis mice by regulating CRH-R2.

改良电抽搐治疗对精神分裂症患者下丘脑激素(CRH和TRH)水平影响的临床对照分析

目的 观察改良电抽搐治疗对精神分裂症患者下丘脑促肾上腺皮质释放激素 (CRH)和促甲状腺激素释放激素 (TRH)的影响。方法 将符合CCMD - 3精神分裂症诊断标准的精神分裂症患者 5 7例随机分为治疗组(30例 )与对照组 (2 7例 )进行观察。用放射免疫分析法分别对两组治疗前、后的CRH和TRH水平进行测定。结果 在治疗后TRH水平治疗组较对照组有明显的降低 ,而CRH在治疗前后变化不明显。结论 改良电抽搐治疗对TRH的影响大于CRH。