亚临床甲状腺功能减退症患者TSH与肾上腺皮质功能的关系

目的分析亚临床甲状腺功能减退症患者促甲状腺激素(TSH)与肾上腺皮质功能的关系。 方法选取150例亚临床甲状腺功能减退症患者为研究组,甲状腺功能正常的健康人群150例为对照组。比较两组TSH、游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)、皮质醇(CORT)和促肾上腺皮质激素(ACTH)水平。采用Pearson法分析亚临床甲状腺功能减退症患者TSH水平与ACTH、CORT水平的相关性。 结果与对照组比较,研究组患者TSH、ACTH水平升高,CORT水平降低(P＜0.05)。Pearson分析结果显示,亚临床甲状腺功能减退症患者TSH水平与ACTH水平呈正相关(P＜0.05),与CORT水平呈负相关(P＜0.05)。 结论亚临床甲状腺功能减退症患者血清TSH水平与肾上腺皮质功能指标ACTH、CORT水平存在相关性。     

白松片对慢性应激抑郁模型大鼠行为学及血浆CORT、ACTH的影响

目的：观察白松片对慢性应激抑郁大鼠模型行为学和血浆CORT、ACTH含量的影响。方法：SD雄性大鼠28只随机分为空白对照组、模型对照组、氟西汀对照组及白松片试验组，选用慢性轻度不可预见性应激加孤养造模，观察各组大鼠敞箱实验和液体消耗等行为学指标变化，采用放射免疫方法检测大鼠血浆皮质醇(CORT)和促肾上腺皮质激素(ACTH)含量。结果：慢性应激抑郁大鼠体重增加缓慢，敞箱实验中的水平运动、垂直运动得分、清洁动作次数显著减少，中央格停留时间显著延长；糖水消耗明显下降，纯水消耗显著增多，而且其血浆皮质醇和促肾上腺皮质激素含量增加。氟西汀和白松片均显著改善慢性应激抑郁大鼠模型的行为学和神经内分泌变化。结论：慢性轻度不可预见性应激可使大鼠行为及神经内分泌发生异常改变，引起抑郁状态，白松片对此具有一定拮抗作用。     

外源性褪黑素对慢性应激抑郁模型大鼠行为学及血清相关激素含量的影响

目的通过观察不同剂量的外源性褪黑素对慢性应激抑郁模型大鼠行为学及血清中5-HT、CRH、ACTH、CORT含量的影响,探讨外源性褪黑素对抑郁症的治疗作用。方法 48只SD大鼠随机分为4组:空白对照组、模型对照组、褪黑素高剂量组、褪黑素低剂量组,每组12只。采用慢性轻度不可预见性应激和孤养方法复制慢性应激抑郁模型,灌胃给予治疗组不同剂量(5.0、10.0 mg·kg-1)的褪黑素加以干预,以体重、糖水试验、旷野试验观察实验前后大鼠行为学的改变。应用酶联免疫吸附法对大鼠血清中5-HT、CRH、ACTH、CORT的含量进行检测。结果从第7天开始,模型组、褪黑素低量组、褪黑素高剂量组的体重增长趋势开始降低,从第14天开始,模型对照组大鼠体重有下降趋势;从第14天开始褪黑素低剂量组、褪黑素高剂量组的糖水摄入量增长趋势降低,模型对照组的糖水摄入量呈下降趋势;第21天,与模型对照组相比,褪黑素低剂量和褪黑素高剂量组大鼠的水平和垂直运动次数都有显著性增多。与空白对照组相比,模型对照组血清5-HT的含量降低、血清CRH、ACTH、CORT含量升高,与模型对照组相比,褪黑素低剂量组和褪黑素高剂量组的血清5-HT含量均显著升高,血清CRH、CORT、ACTH含量均显著降低。结论外源性褪黑素对慢性应激抑郁模型大鼠抑郁行为有改善作用,也可以提高慢性应激抑郁模型大鼠血清中5-HT的含量,降低慢性应激抑郁模型大鼠血清中CRH、ACTH、CORT的含量,但它们之间的具体量效关系有待进一步研究。     

葛根复方对创伤应激大鼠神经内分泌的调整作用

目的:观察创伤应激(PTSD)对大鼠神经内分泌和行为学的影响以及葛根复方制剂的调治作用。方法:建立大鼠创伤应激模型,采用放射免疫方法(RIA)检测大鼠血浆皮质醇(CORT)和促肾上腺皮质激素(ACTH)含量;以旷场实验和鼠尾悬挂实验研究创伤应激对大鼠行为学的影响。结果:创伤应激大鼠血浆CORT和ACTH含量分别为(16.76±2.33)ng/mL和(101.21±22.07)pg/mL,水平运动次数和垂直运动次数分别为(26.2±8.4)次和(8.5±3.5)次,悬尾不动时间(227.00±50.13)s;葛根复方高、中、低剂量组血浆CORT含量为(8.69±2.47),(10.32±2.12)和(12.03±3.06)ng/mL,ACTH含量为(66.63±15.34),(77.49±14.63)和(87.93±12.16)pg/mL,水平运动次数分别为(60.3±13.6),(47.0±11.6)和(34.3±8.2)次,垂直运动次数分别为(24.0±5.5),(20.9±5.8)和(11.5±4.4)次,悬尾不动时间(164.60±46.50),(178.30±38.05)和(195.10±50.61)s。结论:创伤应激可使大鼠神经内分泌及行为发生异常改变,葛根复方制剂对此具有一定的调治作用。     

异常黑胆质载体动物模型的下丘脑-垂体-肾上腺轴功能紊乱的物质基础研究

目的:观察异常黑胆质载体动物模型下丘脑-垂体-肾上腺轴(HPAA)有关指标的变化,探求异常黑胆质载体动物模型HPAA功能紊乱的物质基础。方法:采用干寒饲养环境、干寒属性的饲料饲养、慢性间断足底电击等多因素复制小鼠异常黑胆质载体动物模型,用ELISA法检测血清ACTH、CORT和-βEP含量;采用高效液相-荧光检测分析法分析血清和脑去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)3、、4二羟基本乙酸(DOPAC)等单胺类神经递质含量。结果:血清ACTH、CORT和-βEP含量增加(P<0.05);异常黑胆质载体动物模型血清中NE含量明显增加(P<0.05),DA含量下降(P<0.05),5-HT(P<0.01)和DOPAC(P<0.01)含量减少;脑组织中NE含量明显增加(P<0.05),DA含量减少(P<0.05)和DOPAC含量降低(P<0.01),5-HT含量改变不明显(P>0.05)。结论:异常黑胆质载体动物模型实验动物下丘脑、垂体和肾上腺合成、分泌及调控功能紊乱,下丘脑-垂体-肾上腺轴(HPAA)处于应激激活状态,血清及脑组织单胺类神经递质存在异常。此可能是异常黑胆质载体动物模型存在HPAA紊乱的物质基础。     

急性热应激对大鼠血清ACTH及CORT水平的影响

目的 探讨急性热应激对大鼠血清促肾上腺皮质激素(ACTH)及皮质醇(CORT)水平的影响.方法 选用雄性Wistar大鼠,随机分为对照组与热暴露组,对照组室温为24℃,热暴露组室温为32℃.经7d热暴露后,分别测定大鼠脑垂体与肾上腺的相对质量,采用体温遥感技术检测大鼠体温变化,通过放射免疫法检测ACTH、CORT水平.结果 与对照组相比,急性热应激对大鼠体核温度和体质量影响差异无统计学意义(P＞0.05),而大鼠脑垂体和肾上腺的相对质量增加(P＜0.05),大鼠ACTH、CORT水平升高(P＜0.05).结论 急性热应激可通过升高ACTH、CORT水平,激活下丘脑-垂体-肾上腺皮质轴(HPA)途径调控应激反应.     

Changes of behavioral parameters during long-term food restriction in middle-aged Wistar rats

Food restriction (FR) has a beneficial effect on aging process and exerts a significant effect on the responses of rodents to standard behavioral tasks. The aim of this study was to assess the cumulative influence of FR on the behavioral and biochemical parameters in Wistar rats. Six-month-old rats were subjected to restrictive feeding (50% of the daily food intake, every-other-day feeding regimen) for one month or for six months until ages of 7 and 12 months, respectively. We examined the habituation of exploratory movement, amphetamine (AMPH)-induced motor activity, as well as changes in serum corticosterone (CORT) and glucose levels. The results obtained from FR animals were compared with ad libitum (AL)-fed age-matched control rats. Habituation of motor activity was only affected by six months of restrictive feeding. The sensitization of the motor response to AMPH that was observed in animals exposed to FR for one month was not observed in animals that were exposed to the same feeding regimen for six months. Serum CORT was increased and serum glucose was decreased in both FR groups. These results clearly show that despite the similarity of the biochemical changes that were induced by one and six months of FR, the nature of the changes in motor activities in these two groups of animals during habituation and after AMPH treatment was different. Our findings indicate that long-term FR has complex behavioral consequences that need to be carefully evaluated with respect to animal age, duration of FR and severity of the diet.     

热敏灸对失眠大鼠模型血清内分泌激素水平的影响

目的：观察热敏灸对失眠大鼠模型血清促肾上腺皮质激素（ACTH）、皮质酮（CORT）、甲状腺素（T4）、生长激素（GH）和褪黑素（MT）水平的影响,了解热敏灸治疗失眠的机制.方法：雄性SD大鼠32只,随机分为4组：正常组、模型组、艾灸组和热敏灸组,每组8只.采用腹腔注射对氯苯丙氨酸（PCPA）制备失眠大鼠模型,用Ethovision XT视频跟踪系统录制大鼠活动观察大鼠的行为学表现,用放射免疫分析法检测大鼠血清中ACTH、CORT、T4、GH和MT的水平.结果：与正常组相比,模型组大鼠昼夜节律消失;血清CORT、T4、GH和MT含量均升高,而血清中ACTH含量下降.与模型组相比,热敏灸组大鼠昼夜活动节律基本恢复正常;血清CORT、T4、GH和MT含量均下降,而血清中ACTH含量有所升高.结论：热敏灸能缓解失眠大鼠症状,可能与调节体内激素水平有关.     

Glucocorticoid exposure alters the pathogenesis of Theiler's murine encephalomyelitis virus during acute infection

Previous research has shown that chronic restraint stress exacerbates Theiler's virus infection, a murine model for CNS inflammation and multiple sclerosis. The current set of experiments was designed to evaluate the potential role of glucocorticoids in the deleterious effects of restraint stress on acute CNS inflammatory disease. Exposure to chronic restraint stress resulted in elevated levels of corticosterone as well as increased clinical scores and weight loss (Experiment 1). In addition, corticosterone administration alone exacerbated behavioral signs of TMEV-induced sickness (i.e. decreased body weight, increased symptoms of encephalitis, and increased mortality) and reduced inflammation in the CNS (Experiment 2). Infected subjects receiving exogenous corticosterone showed exacerbation of acute phase measures of sickness and severe mortality as well as decreased viral clearance from CNS (Experiment 3). These findings indicate that corticosterone exposure alone is sufficient to exacerbate acute CNS inflammatory disease.