BACKGROUND & AIMS: :Medial preoptic area (MPOA) and ventral bed nucleus of the stria terminalis (VBST) neurons are involved in maternal behavior, but the neural sites to which the maternally relevant neurons project have not been determined. Since MPOA and VBST neurons express Fos during maternal behavior, we used a double-labeling immunocytochemical procedure to detect both Fos and a retrograde tracer, wheat germ agglutinin (WGA), in order to determine where these Fos neurons project. On Day 4 postpartum, fully maternal females were separated from their litters. On Day 5, WGA was iontophoretically injected into one of the following regions known to receive MPOA and/or VBST input: Lateral septum, medial hypothalamus at the level of the ventromedial nucleus, lateral habenula, ventral tegmental area, retrorubral field, or periaqueductal gray. On Day 7, females received a 2-h test with either pups or candy, after which they were perfused and their brains were processed for the detection of Fos and WGA. As expected, females tested with pups had more Fos-containing neurons in the MPOA and VBST than did females tested with candy. After WGA injections into several brain sites, the number of double-labeled cells observed in the MPOA and VBST was greater for the maternal females when compared to the non-maternal females. Therefore, these results pinpointed neural circuits that were activated during maternal behavior. For the maternal females, Fos-containing neurons in the MPOA projected most strongly to the medial hypothalamus at the level of the ventromedial nucleus and to the lateral septum, while Fos-containing neurons in the VBST projected most strongly to the retrorubral field, ventral tegmental area, and medial hypothalamus. Although relatively few MPOA and VBST neurons which expressed Fos during maternal behavior projected to the periaqueductal gray, these Fos-expressing neurons made up a relatively large proportion of the MPOA and VBST projection to the periaqueductal gray. This study suggests that MPOA and VBST efferents project to a variety of regions to promote full maternal responsiveness.

背景与目标： ：孕产妇的行为涉及视神经内侧视前区（MPOA）和纹状体终末腹侧核（VBST）的母亲行为，但尚未确定与母亲相关的神经元投射到的神经部位。由于MPOA和VBST神经元在孕产妇行为期间表达Fos，因此我们使用双重标记免疫细胞化学方法检测Fos和逆行示踪剂小麦胚芽凝集素（WGA），以确定这些Fos神经元的位置。在产后第4天，将完全产妇的母猪从其产仔中分离出来。在第5天，将WGA离子电渗注入已知可接收MPOA和/或VBST输入的以下区域之一：外侧中隔，腹侧内侧丘脑，腹侧核，腹侧被膜区，腹侧被盖区，后睑缘视野或导水管周围灰色。在第7天，雌性接受幼犬或糖果的2小时测试，然后进行灌注，并对其大脑进行处理以检测Fos和WGA。不出所料，用幼犬测试的雌性在MPOA和VBST中的含Fos的神经元要多于用糖果进行测试的雌性。 WGA注射到多个大脑部位后，与非母体雌性相比，母体雌性在MPOA和VBST中观察到的双标记细胞数量更多。因此，这些结果指出了在孕产妇行为中激活的神经回路。对于孕产妇，MPOA中含有Fos的神经元在腹膜内侧核和外侧中隔的投射力最强，而VBST中含有Fos的神经元在后睑内侧，腹侧被膜的投射力最强。区域和内侧下丘脑。尽管在产妇行为期间表达Fos的MPOA和VBST神经元相对较少，但会投射到导水管周围的灰色，但这些表达Fos的神经元占MPOA和VBST投射至导水管周围的灰色的比例相对较大。这项研究表明，MPOA和VBST传出可投射到各个区域，以促进全面的孕产妇反应。

BACKGROUND & AIMS: :Statins are increasingly being used for the treatment of a variety of conditions beyond their original indication for cholesterol lowering. We previously reported that simvastatin increased dopamine receptors in the rat prefrontal cortex [Q. Wang, W.L. Ting, H. Yang, P.T. Wong, High doses of simvastatin upregulate dopamine D(1) and D(2) receptor expression in the rat prefrontal cortex: possible involvement of endothelial nitric oxide synthase, Br. J. Pharmacol. 144 (2005) 933-939] and restored its downregulation in a model of Parkinson's disease (PD) [Q. Wang, P.H. Wang, C. McLachlan, P.T. Wong, Simvastatin reverses the downregulation of dopamine D1 and D2 receptor expression in the prefrontal cortex of 6-hydroxydopamine-induced Parkinsonian rats, Brain Res. 1045 (2005) 229-233]. Here we explore the effects of simvastatin treatment on tissue dopamine content and reuptake. Sprague-Dawley rats were given simvastatin (1 and 10 mg kg(-1)day(-1), p.o.) for 4 weeks. Brain tissue from prefrontal cortex and striatum were taken out for dopamine content and its reuptake. Using high-performance liquid chromatographic-mass spectrometer (HPLC-MS), simvastatin (10 mg kg(-1)day(-1)) was found to increase dopamine content by 110% in the striatum but decreased by 76% in the prefrontal cortex compared with the saline treated group. Dopamine (DA) reuptake was unchanged in both brain regions. These results suggest that chronic treatment with high dose of simvastatin may affect DA tissue level in prefrontal cortex and striatum without changing on DA reuptake. This may have important clinical implications in psychiatric and striatal dopaminergic disorders.

背景与目标： 他汀类药物已被用于治疗多种疾病，这些症状超出了降低胆固醇的最初指标。我们先前曾报道辛伐他汀会增加大鼠前额叶皮层中的多巴胺受体[Q.王伟丁宏阳黄，辛伐他汀大剂量上调大鼠前额叶皮层中的多巴胺D（1）和D（2）受体表达：可能与内皮一氧化氮合酶Br有关。 J.Pharmacol。 144（2005）933-939]，并在帕金森氏病（PD）模型中恢复了其下调[Q.王凤华Wang C.McLachlan，P.T. Wong，辛伐他汀逆转了6-羟基多巴胺诱导的帕金森病大鼠Brain Res的前额叶皮层中多巴胺D1和D2受体表达的下调。 1045（2005）229-233]。在这里，我们探讨辛伐他汀治疗对组织多巴胺含量和再摄取的影响。 Sprague-Dawley大鼠接受辛伐他汀（1和10 mg kg（-1）day（-1），口服）4周。取出前额叶皮层和纹状体的脑组织中的多巴胺含量并重新摄取。使用高效液相色谱质谱仪（HPLC-MS），发现辛伐他汀（10 mg kg（-1）day（-1））在纹状体中可使多巴胺含量增加110％，但在前额叶中减少76％皮层与生理盐水处理组相比。在两个大脑区域，多巴胺（DA）的再摄取均未改变。这些结果表明，高剂量辛伐他汀的长期治疗可能会影响额叶前额叶皮层和纹状体中的DA组织水平，而不会改变DA的再摄取。这在精神病和纹状体多巴胺能障碍中可能具有重要的临床意义。

BACKGROUND & AIMS: UNLABELLED:The objective of the present study was to investigate whether the endogenous opioids are involved in the control of endothelin-1 release from the pituitary gland. To test this hypothesis we have measured the peripheral plasma concentration of ET-1 as well as the content of immunoreactive ET-1 (irET-1) in the pituitary in response to opioid receptors blockade in euhydrated and 24 h water-deprived Wistar-Kyoto rats. Placebo or naltrexone (50 micrograms/kg body wt.) were given i.v. in both groups. Trunk blood was collected to determine hematocrit, plasma sodium and ET-1 levels (RIA). Immunostaining of ET-1 in the whole pituitary glands was performed by colloidal gold labeling. The quantitative analysis of irET-1 was carried out under a light microscope using a computerized image analyzer (MultiScan). RESULTS:(1) Twenty-four-hour dehydration resulted in marked increase of peripheral concentration of ET-1. Naltrexone injection induced a significant elevation of ET-1 plasma concentration in both, dehydrated and control animals. (2) The content of irET-1 in anterior and intermediate lobes of the pituitary in dehydrated rats was markedly higher than in control group. (3) Naltrexone injection caused a rapid and significant reduction irET-1 within the anterior, intermediate and posterior lobes in dehydrated and control animals. CONCLUSIONS:(1) An elevation of irET-1 in the pituitary gland and peripheral circulation in dehydrated animals may play a role in maintaining of water-electrolyte balance. (2) The mu-opioid system appears to control the ET-1 release from the pituitary in normal and dehydrated animals.

背景与目标： 未标记：本研究的目的是调查内源性阿片类药物是否参与垂体中内皮素-1的释放。为了检验这一假设，我们测量了在无水和缺水24小时的Wistar-Kyoto中阿片受体阻滞后垂体中ET-1的外周血浆浓度以及免疫反应性ET-1（irET-1）的含量大鼠。静脉注射安慰剂或纳曲酮（50微克/千克体重）。在两组中。收集躯干血液以确定血细胞比容，血浆钠和ET-1水平（RIA）。 ET-1在整个垂体中的免疫染色是通过胶体金标记进行的。使用计算机图像分析仪（MultiScan）在光学显微镜下对irET-1进行定量分析。
结果：（1）脱水24小时导致ET-1的外周血浓度明显升高。纳曲酮注射液在脱水和对照动物中均引起ET-1血浆浓度的显着升高。 （2）脱水大鼠垂体前叶和中间叶中irET-1的含量明显高于对照组。 （3）纳曲酮注射液导致脱水和对照动物的前叶，中叶和后叶内的irET-1迅速大量降低。
结论：（1）脱水动物垂体中irET-1的升高和外周循环可能在维持水电解质平衡中发挥了作用。 （2）在正常和脱水动物中，μ阿片样物质系统似乎可以控制ET-1从垂体的释放。

BACKGROUND & AIMS: :Isolated adrenal cells from Vitamin E-deficient and control rats were prepared by a trypsin digestion method. Cyclic adenosine 3',5'-monophosphate (cyclic AMP) formation was studied in response to adrenocorticotropin (ACTH) in the presence and absence of ascorbate by measuring the conversion of prelabeled adenosine 5'-triphosphate [14C]ATP to cyclic [14C]AMP. Ascorbate (0.5 mM) inhibited ACTH-induced cyclic [14C]AMP formation in adrenal cells isolated from Vitamin E-deficient rats but had no effect in the control cells. The inhibitory effect of ascorbate on ACTH-induced cyclic AMP formation in Vitamin E-deficient rats decreased as the concentration of ACTH increased. In Vitamin E-deficient rats ascorbate inhibited ACTH-induced cyclic [14C]AMP formation after 30 min of incubation. There was no further significant accumulation of cyclic [14C]AMP at 60 min or 120 min although in the absence of ascorbate cyclic [14C]AMP continued to be formed. The in vitro addition of alpha-tocopherol reduced the inhibition of ACTH-induced cyclic [14C]AMP formation by ascorbate in Vitamin E-deficient rats. These studies suggest that alpha-tocopherol and ascorbate may affect ACTH-induced cyclic AMP formation through interaction with the membrane-bound enzyme adenylate cyclase.

背景与目标： ：通过胰蛋白酶消化方法，从维生素E缺乏症和对照大鼠中分离出肾上腺细胞。通过测量预先标记的5'-三磷酸腺苷[14C] ATP向环状[14C]的转化，研究了存在和不存在抗坏血酸时对肾上腺皮质激素（ACTH）的响应，研究了环状腺苷3'，5'-单磷酸（环状AMP）的形成AMP。抗坏血酸（0.5 mM）抑制ACTH诱导的从维生素E缺乏症大鼠分离的肾上腺细胞中环[14C] AMP的形成，但对对照细胞没有作用。随着ACTH浓度的增加，抗坏血酸对ACTH诱导的维生素E缺乏症大鼠环AMP形成的抑制作用降低。在维生素E缺乏的大鼠中，孵育30分钟后，抗坏血酸会抑制ACTH诱导的环状[14C] AMP的形成。尽管在不存在抗坏血酸盐的情况下仍继续形成环状[14C] AMP，但在60分钟或120分钟时没有进一步显着的环状[14C] AMP蓄积。在维生素E缺乏的大鼠中，体外添加α-生育酚可降低抗坏血酸对ACTH诱导的环[14C] AMP形成的抑制作用。这些研究表明，α-生育酚和抗坏血酸可能通过与膜结合酶腺苷酸环化酶相互作用而影响ACTH诱导的环AMP的形成。

BACKGROUND & AIMS: -2

背景与目标： -2

BACKGROUND & AIMS: OBJECTIVE:The aim of the present investigation was to characterize the effects of supraphysiological doses of the anabolic androgenic steroid nandrolone decanoate (ND) on the fertility of female rats, as well as on the morphology of their uterus. STUDY DESIGN:Female Wistar rats (n=15) received a subcutaneous injection of ND (15 mg/kg) once daily during a 2-week period, while the control animals (n=10) were administered vehicle alone (arachidis oleum) in the same manner. Estrus behavior was evaluated 4 weeks after termination of this treatment and in cases where signs of receptivity were present, the female rat was given the opportunity to copulate with a male. After breeding, the female animals were sacrificed and their uteri examined histomorphologically. RESULTS:All ND-treated animals exhibited abnormal vaginal smears, whereas all of the control smears were normal. Most (73%) of the treated females demonstrated normal estrus behavior (i.e., willingness) on the day of mating, but none got pregnant; whereas all of the control rats became pregnant. The female rats receiving the ND showed an enhanced rate of weight gain and the myometrium thickness of their uteri was significantly increased, while the endometrium was significantly thinner. Furthermore, ND caused a significant proportion of the treated animals to display tortuous and irregularly branching endometrial glands, as well as a lack of the physiologically normal infiltration of eosinophilic leukocytes into the endometrium (endometrial eosinophilic homing), a finding that has not been reported previously. CONCLUSION:The present findings indicate that high doses of ND cause morphological and physiological alterations in the uterus of female rats that are associated with a suppression of their reproductive capacity.

背景与目标： 目的：本研究的目的是表征同化雄性类固醇癸酸nandrolone癸酸酯的超生理剂量对雌性大鼠生育能力以及子宫形态的影响。
研究设计：Wistar雌性大鼠（n = 15）在2周内每天一次皮下注射ND（15 mg / kg），而对照组（n = 10）单独给予媒介物（花生油）。同样的方式。终止该治疗4周后评估发情行为，并且在出现接受迹象的情况下，给予雌性大鼠与雄性交配的机会。繁殖后，将雌性动物处死并对其子宫进行组织形态学检查。
结果：所有接受ND治疗的动物均表现出异常的阴道涂片，而所有对照涂片均正常。接受治疗的大多数女性（73％）在交配当天表现出正常的发情行为（即意愿），但没有人怀孕；而所有对照大鼠都怀孕了。接受ND的雌性大鼠体重增加率增加，子宫肌层厚度明显增加，而子宫内膜明显变薄。此外，ND导致相当一部分被治疗的动物表现出曲折和不规则分支的子宫内膜腺体，并且缺乏正常的嗜酸性白细胞进入子宫内膜的生理正常浸润（子宫内膜嗜酸性归巢），这一发现此前尚未见报道。 。
结论：本研究结果表明，高剂量的ND可导致雌性大鼠子宫形态和生理改变，从而抑制其生殖能力。

BACKGROUND & AIMS: :We studied the influence of aprotinin and soya bean trypsin inhibitor (SBTI) on the inflammatory reaction induced by the implantation of dry sponges in normal Wistar rats and in kininogen-deficient Brown Norway rats, during the first day after the implantation. In normal rats, aprotinin reduced the volume and total protein content of the exudates at 3 h but not thereafter. Aprotinin also markedly reduced the immunoreactive kinins and kallikrein in the exudates. Aprotinin did not modify the volume of the exudates of the Brown Norway rats. SBTI reduced the inflammatory reaction in both rat strains but did not significantly modify the formation of immunoreactive kinins. The inflammatory reaction developed more slowly in Brown Norway rats. The kinin system is thus involved during the first hours of the development of this acute inflammatory reaction. The anti-inflammatory effect of SBTI does not depend on the inhibition of kinin formation.

背景与目标： ：我们研究了抑肽酶和大豆胰蛋白酶抑制剂（SBTI）在植入后第一天对正常Wistar大鼠和缺乏激肽原的褐挪威大鼠中植入干海绵诱导的炎症反应的影响。在正常大鼠中，抑肽酶在3 h时减少了渗出液的体积和总蛋白含量，但此后没有降低。抑肽酶还显着降低了渗出液中的免疫反应激肽和激肽释放酶。抑肽酶未改变棕色挪威大鼠渗出液的体积。 SBTI减少了两种大鼠品系中的炎症反应，但并未显着改变免疫反应激肽的形成。在布朗挪威大鼠中，炎症反应发展得较慢。因此，激肽系统参与了这种急性炎症反应发展的最初几个小时。 SBTI的抗炎作用不取决于对激肽形成的抑制作用。

BACKGROUND & AIMS: :Severe iodine deficiency is characterized by goiter, preferential synthesis, and secretion of T(3) in thyroids, hypothyroxinemia in plasma and tissues, normal or low plasma T(3), and slightly increased plasma TSH. We studied changes in deiodinase activities and mRNA in several tissues of rats maintained on low-iodine diets (LIDs) or LIDs supplemented with iodine (LID+I). T(4) and T(3) concentrations decreased in plasma, tissues, and thyroids of LID rats, and T(4) decreased more than T(3) (50%). The highest type 1 iodothyronine deiodinase (D1) activities were found in the thyroid, kidney, and the liver; pituitary, lung, and ovary had lower D1 activities; but the lowest levels were found in the heart and skeletal muscle. D1 activity decreased in all tissues of LID rats (10-40% of LID+I rats), except for ovary and thyroids, which D1 activity increased 2.5-fold. Maximal type 2 iodothyronine deiodinase (D2) activities were found in thyroid, brown adipose tissue, and pituitary, increasing 6.5-fold in thyroids of LID rats and about 20-fold in the whole gland. D2 always increased in response to LID, and maximal increases were found in the cerebral cortex (19-fold), thyroid, brown adipose tissue, and pituitary (6-fold). Lower D2 activities were found in the ovary, heart, and adrenal gland, which increased in LID. Type 3 iodothyronine deiodinase activity was undetectable. Thyroidal Dio1 and Dio2 mRNA increased in the LID rats, and Dio1 decreased in the lung, with no changes in mRNA expression in other tissues. Our data indicate that LID induces changes in deiodinase activities, especially in the thyroid, to counteract the low T(4) synthesis and secretion, contributing to maintain the local T(3) concentrations in the tissues with D2 activity.

背景与目标： ：严重的碘缺乏症的特征是甲状腺肿大，甲状腺的优先合成和分泌T（3），血浆和组织中的甲状腺素低血症，血浆T（3）正常或较低以及血浆TSH略有增加。我们研究了低碘饮食（LIDs）或补充碘的LID（LID I）维持的大鼠几个组织中脱碘酶活性和mRNA的变化。在LID大鼠的血浆，组织和甲状腺中，T（4）和T（3）的浓度降低，而T（4）的降低幅度大于T（3）（50％）。在甲状腺，肾脏和肝脏中发现最高的1型碘甲状腺素脱碘酶（D1）活性。垂体，肺和卵巢的D1活性较低；但是最低的水平是在心脏和骨骼肌中发现的。除卵巢和甲状腺外，LID大鼠所有组织中的D1活性均降低（LID I大鼠的10-40％），D1活性提高了2.5倍。在甲状腺，褐色脂肪组织和垂体中发现最大的2型碘甲状腺素脱碘酶（D2）活性，在LID大鼠的甲状腺中增加了6.5倍，在整个腺体中增加了约20倍。 D2总是响应LID而增加，在大脑皮层（19倍），甲状腺，褐色脂肪组织和垂体（6倍）中发现最大的增加。在卵巢，心脏和肾上腺中发现较低的D2活性，而LID升高。无法检测到3型碘甲状腺素脱碘酶活性。 LID大鼠的甲状腺Dio1和Dio2 mRNA增加，而肺中Dio1减少，其他组织的mRNA表达没有变化。我们的数据表明，LID诱导脱碘酶活性的变化，尤其是在甲状腺中，以抵消低T（4）的合成和分泌，从而有助于维持具有D2活性的组织中的局部T（3）浓度。

BACKGROUND & AIMS: RATIONALE:There is a need for improved therapeutic interventions to treat both drug- and sleep-induced respiratory depression. Increased understanding of the neurochemical control of respiration will help identify a basis for advances. Activation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors positively modulates respiratory drive and rhythmogenesis in several brain regions including the pre-Bötzinger complex. Ampakines are a diverse group of small molecules that activate subsets of these receptors. OBJECTIVE:We determined whether the ampakine CX546 would enhance respiratory drive and rhythmogenesis across various stages of development and whether this ampakine could counter opioid- and barbiturate-induced respiratory depression. METHODS:Respiratory frequency and amplitude were measured in the following rat models: (1) perinatal in vitro brainstem-spinal cord, (2) neonatal in vitro medullary slice, (3) juvenile in situ perfused, working heart-brainstem preparation, and (4) newborn and adult in vivo. RESULTS:Administration of CX546 stimulated baseline respiratory frequency in perinatal in vitro preparations but not in older animals (greater than Postnatal Day 0). Furthermore, pharmacologic depression of respiratory frequency and amplitude was countered at all ages studied by the administration of CX546 in vitro, in situ, and in vivo. Significantly, CX546 countered opioid-induced breathing depression in all preparations, without altering analgesia as assessed by measuring the time to foot withdrawal in response to a thermal stimulus. CONCLUSIONS:CX546 effectively reverses opioid- and barbiturate-induced respiratory depression without reversing the analgesic response. These studies suggest that ampakines may be useful in preventing or reversing opioid-induced respiratory depression and identify the potential of ampakines for alleviating other forms of respiratory depression including sedative use and sleep apnea.

背景与目标： 理由：有必要改善治疗干预措施，以治疗药物和睡眠诱发的呼吸抑制。对呼吸的神经化学控制的更多了解将有助于确定进展的基础。 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）型谷氨酸受体的激活可正向调节包括伯森格前体在内的多个大脑区域的呼吸驱动和节律。苯丙胺类化合物是激活这些受体子集的各种小分子。
目的：我们确定了安帕卡因CX546是否在整个发育的各个阶段都可以增强呼吸驱动和节律，并且该安帕卡因是否可以抵抗阿片类药物和巴比妥酸盐引起的呼吸抑制。
方法：在以下大鼠模型中测量呼吸频率和振幅：（1）围产期体外脑干-脊髓，（2）新生儿体外髓质片，（3）幼年原位灌注，正常工作的心脑干，和4）新生儿和成人体内。
结果：在围产期体外制剂中施用CX546刺激了基线呼吸频率，但在年长动物中则没有（大于出生后第0天）。此外，通过研究在体外，原位和体内施用CX546，在所有年龄的研究中都可以抵消呼吸频率和振幅的药理抑制作用。值得注意的是，CX546在所有制剂中均能抵抗阿片类药物引起的呼吸抑制，而无需改变镇痛效果（通过测量对热刺激的撤退时间来评估镇痛效果）。
结论：CX546可有效逆转阿片类药物和巴比妥类药物引起的呼吸抑制，而不会逆转镇痛反应。这些研究表明，安帕他酮可能在预防或逆转阿片类药物引起的呼吸抑制中有用，并确定了安帕可酮缓解其他形式的呼吸抑制的潜力，包括镇静使用和睡眠呼吸暂停。

BACKGROUND & AIMS: BACKGROUND:Diabetes mellitus (DM) is associated with hyperglycemia, inflammatory disorders and abnormal lipid profiles, currently the extracts from leaves of cynara scolymus has been discovered to treat metabolic disorders and has been stated by multitudinous scientists according to a good source of polyphenols compounds. The present study aimed to evaluate the protective effect of the ethanol leaves extract of C. scolymus in alloxan induced stress oxidant, hepatic-kidney dysfunction and histological changes in liver, kidney and pancreas of different experimental groups of rats. METHODS:We determinate the antioxidant activity by ABTS .+ and antioxidant total capacity (TAC) of all extracts of C. scolymus leaves, the inhibition of α-amylase activity in vitro was also investigated. Forty male Wistar rats were induced to diabetes with a single dose intraperitoneal injection (i.p.) of alloxan (150 mg/kg body weight (b.w.)). Diabetic rats were orally and daily administrated of ethanol extract from C. scolymus at two doses (200-400 mg/kg, b.w) or (12 mg/kg, b.w) with anti-diabetic reference drug, Acarbose for one month. Ethanol extract of C. scolymus effect was confirmed by biochemical analysis, antioxidant activity and histological study. RESULTS:The results indicated that the ethanol extract from leaves of C. scolymus showed the highest antioxidant activity by ABTS .+ (499.43g± 39.72 Trolox/g dry extract) and (128.75 ± 8.45 mg VC /g dry extract) for TAC and endowed the powerful inhibition in vitro of α-amylase activity with IC50=72,22 ug/uL. In vivo, the results showed that ethanol extract from the leaves of C. scolymus (200-400 mg/kg) decreased significantly (p < 0.001) the α-amylase levels in serum of diabetic rats, respectively associated with significant reduction (p < 0.001) in blood glucose rate of 42,84% and 37,91% compared to diabetic groups after 28 days of treatment, a significant lowered of plasma total cholesterol (T-Ch) by 18,11% and triglyceride (TG) by 60,47%, significantly and low-density lipoproteins (LDL-C) by 37,77%, compared to diabetic rats, moreover, the administration of ethanol extract appears to exert anti-oxidative activity demonstrated by the increase of CAT, SOD and GSH activities in liver, kidney and pancreas of diabetic rats. This positive effect of the ethanol extract from C. scolymus was confirmed by histological study. CONCLUSION:These observed strongly suggest that ethanol extract from the leaves of C. scolymus has anti-hyperglycemic properties, at least partly mediated by antioxidant and hypolipidemic effects.

背景与目标： 背景：糖尿病（DM）与高血糖，炎性疾病和异常脂质状况相关，目前已发现粘虫c叶片的提取物可治疗代谢紊乱，许多科学家已经根据多酚化合物的良好来源进行了陈述。本研究旨在评价鳞球菌乙醇叶提取物对四氧嘧啶诱导的应激氧化剂，肝肾功能障碍以及不同实验组大鼠肝，肾和胰腺组织学变化的保护作用。
方法：我们通过ABTS测定抗氧化活性。鼠尾草叶片的所有提取物的抗氧化剂和总抗氧化剂（TAC），还研究了其对α-淀粉酶活性的体外抑制作用。通过单剂量腹膜内注射（i.p.）四氧嘧啶（150 mg / kg体重（b.w.））将40只雄性Wistar大鼠诱发为糖尿病。糖尿病大鼠口服和每天服用两种剂量（200-400 mg / kg，b.w）或（12 mg / kg，b.w）的鼠尾草乙醇提取物和抗糖尿病参考药物阿卡波糖（acarbose）。通过生化分析，抗氧化活性和组织学研究证实了粘液梭状芽胞杆菌的乙醇提取物作用。
结果：结果表明，ABTS从粘枝sco叶片中提取的乙醇具有最高的抗氧化活性。 （499.43g±39.72 Trolox / g干提取物）和（128.75±8.45 mg VC / g干提取物）用于TAC，并在体外有效抑制α-淀粉酶活性，IC50 = 72.22 ug / uL。在体内，结果显示，从粘液梭菌的叶子中提取乙醇（200-400 mg / kg）显着降低（p <0.001）糖尿病大鼠血清中的α-淀粉酶水平，分别与显着降低有关（p <0.001）。在治疗28天后，与糖尿病组相比，血糖比率分别为0.001、42.84％和37.91％，血浆总胆固醇（T-Ch）显着降低了18.11％，甘油三酸酯（TG）显着降低了60与糖尿病大鼠相比，低密度脂蛋白（LDL-C）降低了47.7％，低密度脂蛋白（LDL-C）降低了37.77％，此外，乙醇提取物的给药似乎表现出抗氧化活性，这是由于CAT，SOD和GSH的增加所证明的在糖尿病大鼠肝，肾和胰腺中的活性。组织学研究证实了粘液梭菌乙醇提取物的这种积极作用。
结论：这些观察结果强烈表明，从粘液梭菌的叶子中提取乙醇具有抗降血糖作用，至少部分是由抗氧化剂和降血脂作用介导的。

BACKGROUND & AIMS: :The transection of the inferior alveolar nerve (IANx) produces allodynia in the whisker pad (V2 division) of rats. Ectopic discharges from injured trigeminal ganglion (TG) neurons and thalamocortical reorganization are possible contributors to the sensitization of uninjured V2 primary and CNS neurons. To test which factor is more important, TG and ventroposterior medial nucleus (VPM) neurons were longitudinally followed before, during, and after IANx for up to 80 d. Spontaneous discharges and mechanical stimulation-evoked responses were recorded in conscious and in anesthetized states. Results show (1) a sequential increase in spontaneous activities, first in the injured TG neurons of the IAN (2-30 d), followed by uninjured V2 ganglion neurons (6-30 d), and then VPM V2 neurons (7-30 d) after IANx; (2) ectopic discharges included burst and regular firing patterns in the IAN and V2 branches of the TG neurons; and (3) the receptive field expanded, the modality shifted, and long-lasting after-discharges occurred only in VPM V2 neurons. All of these changes appeared in the late or maintenance phase (7-30 d) and disappeared during the recovery phase (40-60 d). These observations suggest that ectopic barrages in the injured IAN contribute more to the development of sensitization, whereas the modality shift and evoked after-discharges in the VPM thalamic neurons contribute more to the maintenance phase of allodynia by redirecting tactile information to the cortex as nociceptive.

背景与目标： ：下牙槽神经（IANx）横断会在大鼠的晶须垫（V2分区）中产生异常性疼痛。受伤的三叉神经节（TG）神经元的异位放电和丘脑皮质重组可能是未受伤的V2原发神经元和CNS神经元致敏的原因。为了测试哪个因素更重要，在IANx之前，期间和之后纵向跟踪TG和后内侧内侧核（VPM）神经元长达80 d。在有意识和麻醉状态下记录自发放电和机械刺激诱发的反应。结果显示（1）自发活动的顺序增加，首先是IAN受伤的TG神经元（2-30 d），其次是未受伤的V2神经节神经元（6-30 d），然后是VPM V2神经元（7-30） d）在IANx之后； （2）异位放电包括TG神经元IAN和V2分支的爆发和规则放电模式； （3）仅在VPM V2神经元中，感受野扩大，模态改变且持续放电。所有这些变化都出现在后期或维护阶段（7-30 d），而在恢复阶段（40-60 d）则消失了。这些观察结果表明，受伤的IAN的异位弹幕对致敏作用的贡献更大，而VPM丘脑神经元的形态改变和诱发的放电后，则通过将触觉信息重定向至伤害性皮层，从而对异常性疼痛的维持阶段做出了更大贡献。

BACKGROUND & AIMS: :Persistent pulmonary hypertension of the newborn (PPHN) is a life‑threatening disease that is commonly observed in the neonatal intensive care unit. PPHN is pathologically characterized by pulmonary vascular remodeling and, in particular, pulmonary artery smooth muscle cell (PASMC) proliferation. Decreased expression levels of peroxisome proliferator‑activated receptor γ (PPAR‑γ), which is a member of the nuclear receptor hormone superfamily, in combination with elevated expressions of transient receptor potential cation channel, subfamily C, member 1 (TRPC1) and TRPC6 contributes to the PASMC proliferation and excessive pulmonary vascular remodeling in adult pulmonary hypertension (PH). Whether PPAR‑γ, TRPC1 and TRPC6 affect the development of vascular remodeling in PPHN model rats remains unknown. The aim of the present study was to investigate the roles of PPAR‑γ, TRPC1 and TRP6 on the pathogenesis of PPHN in rats. The rat model of PPHN was established by exposure to hypoxic conditions and indomethacin treatment. Lung tissues, hearts and blood from PPHN model and Control rats were collected and examined. Parameters, including the percentage of medial wall thickness (WT %), the percentage of medial wall area (WA %), right ventricular hypertrophy (RVH) and the plasma concentration of B‑type natriuretic peptide (BNP) were used to estimate the development of PPHN. The expression levels of PPAR‑γ, TRPC1 and TRPC6 in lung tissues were detected by immunohistochemistry, western blotting and reverse transcription‑quantitative polymerase chain reaction. Significant increases were observed in the WT %, WA %, RVH and plasma BNP in the PPHN group compare with the Control group (P<0.01). In addition, the mRNA and protein expression levels of PPAR‑γ were markedly downregulated (P<0.05 vs. Control). In the PPHN group, the protein expression levels of TRPC1 and TRPC6 were higher compared to the control group; however, there was no difference in the mRNA expression levels (P>0.05). In conclusion, the present study successfully established a PPHN rat model, and the altered expressions of PPAR‑γ, TRPC1 and TRPC6 in the pulmonary artery located in the lungs of newborn rats with PPHN suggested that these proteins may be important mediators of PPHN.

背景与目标： ：新生儿持续性肺动脉高压（PPHN）是威胁生命的疾病，通常在新生儿重症监护室中观察到。 PPHN的病理特征是肺血管重塑，尤其是肺动脉平滑肌细胞（PASMC）增殖。过氧化物酶体增殖物激活受体γ（PPAR-γ）的表达水平降低，PPAR-γ是核受体激素超家族的成员，与瞬态受体潜在阳离子通道，亚家族C，成员1（TRPC1）和TRPC6的表达升高有关对成人肺动脉高压（PH）中PASMC增殖和过度肺血管重构的影响。 PPAR-γ，TRPC1和TRPC6是否影响PPHN模型大鼠血管重塑的发展尚不清楚。本研究的目的是研究PPAR-γ，TRPC1和TRP6在大鼠PPHN发病中的作用。通过暴露于低氧条件和消炎痛治疗，建立了PPHN大鼠模型。收集并检查PPHN模型和对照组大鼠的肺组织，心脏和血液。使用参数，包括内侧壁厚百分比（WT％），内侧壁面积百分比（WA％），右心室肥大（RVH）和B型利钠肽（BNP）的血浆浓度来评估发育情况PPHN。通过免疫组织化学，Western印迹和逆转录定量聚合酶链反应检测肺组织中PPAR‑γ，TRPC1和TRPC6的表达水平。与对照组相比，PPHN组的WT％，WA％，RVH和血浆BNP显着增加（P <0.01）。此外，PPAR-γ的mRNA和蛋白表达水平显着下调（P <0.05 vs.Control）。 PPHN组的TRPC1和TRPC6的蛋白表达水平高于对照组。然而，mRNA表达水平没有差异（P> 0.05）。总之，本研究成功建立了PPHN大鼠模型，而PPHN新生大鼠肺中肺动脉中PPAR-γ，TRPC1和TRPC6的表达改变表明，这些蛋白可能是PPHN的重要介体。

BACKGROUND & AIMS: PURPOSE:The present study was aimed to evaluate the retinoprotective effects of Moringa oleifera (MO) in Streptozotocin-induced diabetic rats. METHODS:The study was continued for 24 weeks and evaluated for inflammatory (tumor necrosis factor [TNF]-α and interleukin [IL]-1β, angiogenic (vascular endothelial growth factor [VEGF] and protein kinase C [PKC]-β) and antioxidant (Glutathione, Superoxide dismutase, and Catalase) parameters. Retinal leakage was checked by Fluorescein angiography (FA) and fundus photographs were evaluated for retinal vessel caliber (arteriolar and venular). Transmission electron microscopy was done to determine basement membrane (BM) thickness. RESULTS:The results of the present study showed potential hypoglycemic and retinal antioxidant effects of MO. In the present study, a significant rise in the expression of retinal inflammatory (TNF-α and IL-1β) and angiogenic (VEGF and PKC-β) parameters was observed in diabetic retinae as compared to normal retinae. However, MO-treated retinae showed marked inhibition in the expression of inflammatory and angiogenic parameters. Further, in the present study, diabetic retinae showed dilated retinal vessels as compared to normal. However, MO-treated retinae showed marked prevention in the dilatation of retinal vessels. Fluorescein angiograms obtained from diabetic retinae showed leaky and diffused retinal vasculature. On the other hand, MO-treated retinae showed intact retinal vasculature. Further, results of the transmission electron microscopy study showed thickened capillary BM in the diabetic retina as compared to normal retinae. However, treatment with MO prevented thickening of capillary BM. CONCLUSION:Our result suggests that MO may be useful in preventing diabetes induced retinal dysfunction.

背景与目标： 目的：本研究旨在评估辣木（MO）对链脲佐菌素诱导的糖尿病大鼠的视网膜保护作用。
方法：研究持续了24周，并评估了炎症（肿瘤坏死因子[TNF]-α和白介素[IL]-1β]，血管生成（血管内皮生长因子[VEGF]和蛋白激酶C [PKC]-β）和抗氧化剂（谷胱甘肽，超氧化物歧化酶和过氧化氢酶）参数，通过荧光素血管造影（FA）检查视网膜渗漏并评估眼底照片的视网膜血管口径（小动脉和小静脉），用透射电子显微镜确定基底膜（BM）的厚度。
结果：本研究结果显示了MO潜在的降血糖和视网膜抗氧化作用。在本研究中，与正常视网膜相比，在糖尿病视网膜中观察到了视网膜炎症表达（TNF-α和IL-1β）和血管生成（VEGF和PKC-β）参数的显着增加。然而，MO处理的视网膜在炎症和血管生成参数的表达中显示出明显的抑制作用。此外，在本研究中，与正常人相比，糖尿病视网膜显示出视网膜血管扩张。但是，MO处理的视网膜在视网膜血管扩张中显示出明显的预防作用。从糖尿病视网膜获得的荧光素血管造影照片显示渗漏和弥散性视网膜血管系统。另一方面，MO治疗的视网膜显示完整的视网膜脉管系统。此外，透射电子显微镜研究的结果显示与正常视网膜相比，糖尿病视网膜中的毛细血管BM增厚。但是，用MO进行治疗可防止毛细血管BM增厚。
结论：我们的结果表明，MO可能有助于预防糖尿病引起的视网膜功能障碍。

BACKGROUND & AIMS: AIM:To identify the changes of mitochondrial protein expression in diabetic renal parenchyma and to characterize their molecular functions and biological processes in diabetes. METHODS:Mitochondrial proteins extracted from renal parenchyma mitochondria of streptozotocin-induced diabetic rats and normal rats were separated by two-dimensional polyacrylamide gel electrophoresis and identified by matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry. RESULTS:Eleven proteins from 533 visualized protein spots displayed significant different expressions in mitochondria of diabetic kidneys compared with those in normal ones. Among these altered proteins, two proteins with the most obvious changes in protein expression were identified as alpha-2u globulin (mature protein, named A2) and its proteolytically modified form (named A2-fragment) respectively. These proteins were found in mitochondria of male rat renal parenchyma and were proved to be down-regulated in diabetic rats simultaneously. CONCLUSION:Our results suggest that down-regulation of alpha-2u globulin may be associated with an abnormal β-oxidation of long-chain fatty acids during diabetes. The decreased expression of A2-fragment in renal mitochondria of diabetic nephropathy may reduce fatty acid β-oxidation, which leads to a diminished energy supply from mitochondria to kidney tissue and the deposition of a large number of fatty acids in the kidney, ultimately causing and aggravating kidney damage. In conclusion, these findings may be helpful for understanding the molecular mechanism of diabetic nephropathy.

背景与目标： 目的：确定糖尿病肾实质中线粒体蛋白表达的变化，并探讨其在糖尿病中的分子功能和生物学过程。
方法：采用二维聚丙烯酰胺凝胶电泳分离从链脲佐菌素诱发的糖尿病大鼠和正常大鼠的肾实质线粒体中提取的线粒体蛋白，并通过基质辅助激光解吸/电离串联时间质谱法进行鉴定。
结果：533个可视化蛋白斑点中的11种蛋白在糖尿病肾线粒体中的表达与正常肾脏相比明显不同。在这些改变的蛋白质中，两个蛋白质表达变化最明显的蛋白质分别被鉴定为alpha-2u球蛋白（成熟蛋白质，称为A2）及其蛋白水解修饰形式（称为A2片段）。这些蛋白在雄性大鼠肾实质的线粒体中发现，并在糖尿病大鼠中同时被下调。
结论：我们的结果表明，糖尿病患者中α-2u球蛋白的下调可能与长链脂肪酸的β-氧化异常有关。糖尿病肾病肾脏线粒体中A2片段的表达降低可能会降低脂肪酸β氧化，从而导致线粒体向肾脏组织的能量供应减少以及大量脂肪酸在肾脏中的沉积，最终导致和加重肾脏损害。总之，这些发现可能有助于理解糖尿病性肾病的分子机制。

BACKGROUND & AIMS: BACKGROUND:The aim of the present study was to evaluate the effects of low-level laser therapy (LLLT) on the healing of bone defects in rats with streptozotocin (STZ)-induced DM. METHODS:28 male Sprague-Dawley rats were used in this study. 14 animals received a single dose of STZ intraperitoneally (65 mg/kg) to induce Type I DM, whereas others were injected only with sterile saline solution. Four weeks later, standard bone defects were created in the tibiae of rats. Surgical wounds in one group from each of the diabetic and non-diabetic animals were irradiated with diode laser for every other day for 4 weeks and they were described as DM + LLLT and CONT + LLLT groups, respectively. Remaining two groups received no laser treatment. New bone formation, osteoblast and blood vessel counts were calculated in histologic sections. RESULTS:DM group had significantly smaller bone area and lower blood vessel count when compared to DM + LLLT, CONT and CONT + LLLT groups (p < 0.05 for each). CONT and CONT + LLLT groups had significantly larger bone area than DM + LLLT group (p < 0.05 for both). CONCLUSIONS:LLLT application promoted vascularization and new bone formation in animals with DM to a limited extent, since it was unable to support the healing process up to the level of non-diabetic animals.

背景与目标： 背景：本研究的目的是评估低剂量激光疗法（LLLT）对链脲佐菌素（STZ）诱导的DM大鼠骨缺损愈合的作用。
方法：采用28只雄性Sprague-Dawley大鼠。 14只动物腹膜内接受单剂STZ（65 mg / kg）诱导I型DM，而其他动物仅注射无菌盐溶液。四周后，在大鼠胫骨中形成了标准的骨缺损。每隔一天用二极管激光照射来自糖尿病和非糖尿病动物中每组的一组手术伤口，持续4周，分别称为DM LLLT组和CONT LLLT组。其余两组未接受激光治疗。在组织学切片中计算新的骨形成，成骨细胞和血管计数。
结果：与DM LLLT，CONT和CONT LLLT组相比，DM组的骨面积显着更小，血管计数更低（每组p <0.05）。 CONT和CONT LLLT组的骨面积明显大于DM LLLT组（两者均p <0.05）。
结论：LLLT的应用在一定程度上促进了DM动物的血管形成和新骨的形成，因为它不能支持非糖尿病动物的愈合过程。