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。

BACKGROUND & AIMS: :The embryotoxicity/teratogenicity of the sugar replacer isomalt was studied in Wistar rats and New Zealand White rabbits. Groups of 22-23 female rats were given diets containing isomalt at concentrations of 2.5, 5 or 10%, from day 0 to day 21 of pregnancy. The possible adverse effects of restricted feeding were studied in an additional group (food intake less than 80% of the control values). Groups of 36-37 female rabbits were given diets containing isomalt at concentrations of 2.5, 5 or 10%, from day 0 to day 29 of pregnancy. The female rats and rabbits were killed on days 21 and 29 of pregnancy, respectively. In both species no maternal toxicity occurred and no effects on reproductive performance nor on embryonic or foetal development were seen in any of the groups fed isomalt. The feeding of restricted amounts of stock diet to pregnant rats resulted in decreased maternal weight gain and lower uterus weights. Furthermore, this group had an increased number of resorptions and small foetuses, decreased foetus and placental weights and retarded bone development.

背景与目标： ：在Wistar大鼠和新西兰白兔中研究了糖替代品异麦芽酮糖的胚胎毒性/致畸性。从怀孕的第0天到第21天，对22-23只雌性大鼠组给予含异麦芽酮糖的饮食，其浓度为2.5％，5％或10％。在另一组中研究了限制进食的可能的不良影响（食物摄入量少于对照值的80％）。从怀孕的第0天到第29天，给每组36-37只雌性兔子饲喂含有2.5、5％或10％异麦芽酮糖的饮食。雌性大鼠和兔子分别在怀孕的第21天和第29天被杀死。在这两个物种中，没有任何母体毒性发生，并且在饲喂异麦芽酮糖的任何组中均未见对生殖性能，胚胎或胎儿发育有影响。向怀孕的大鼠喂食有限量的基础饮食会导致孕产妇体重增加减少和子宫重量降低。此外，该组的吸收增加，胎儿少，胎儿和胎盘重量减少，骨骼发育受阻。

BACKGROUND & AIMS: :New biomaterials including surface modifications should undergo in vitro and in vivo evaluation before clinical trials. The objective of our in vivo study was to evaluate the biocompatibility of one of the newly fabricated zirconia implant surfaces, called "mds". For this purpose, the osseointegration of these implants was analyzed after implantation in surgically created defects in the cranium of adult male rats. After a healing period of 28 and 56 days, respectively, bone tissue specimens containing the implants were processed and histologically analyzed. For this purpose, sections were stained with haematoxylin/eosin and Masson Goldner trichrome. No signs of cellular inflammatory infiltrate were found in any of the animals. After 28 days, slices showed pronounced development of blood vessels and bone regeneration. After 56 days of healing, direct bridging of the bone defects was detectable with distinctly visible kit lines. There were cell rich areas of connective tissue/bone marrow between zirconia discs and bearing bone. Histomorphometric analysis presented a regenerated bone mean value of 36.3% after 28 days of healing. After 56 days of healing, a 1.6 fold increased bone mean value was observed (58.2%). Using the same analysis, 1% and 39.9% of bone-implant-contact was visible after both healing periods, respectively. On average, connective tissue/marrow spaces occupied 99% of implant-contact-area after 28 days of healing. This area was reduced to 60.1% after 56 days. Within the limits of the animal investigation presented, it was concluded that the tested surface modification of zirconia implants were biocompatible and osseoconductive.

背景与目标： ：包括表面修饰在内的新生物材料应在临床试验之前进行体外和体内评估。我们体内研究的目的是评估一种新制造的氧化锆植入物表面（称为“ mds”）的生物相容性。为了这个目的，在植入成年雄性大鼠的颅骨中手术产生的缺陷后，分析了这些植入物的骨整合。在分别愈合28天和56天之后，对包含植入物的骨组织标本进行了处理并进行了组织学分析。为此，将切片用苏木精/曙红和Masson Goldner三色染色。在任何动物中均未发现细胞炎性浸润的迹象。 28天后，切片显示出明显的血管发育和骨再生。修复56天后，可以使用明显可见的套件线检测到骨缺损的直接桥接。氧化锆椎间盘和承骨之间存在结缔组织/骨髓的细胞富集区域。组织形态计量学分析显示，愈合28天后的骨再生平均值为36.3％。康复56天后，观察到骨平均值增加了1.6倍（58.2％）。使用相同的分析，在两个愈合期之后，分别可见1％和39.9％的骨-植入物接触。平均而言，愈合28天后，结缔组织/骨髓间隙占植入物接触面积的99％。 56天后，该面积减少到60.1％。在提出的动物研究的范围内，得出的结论是，经测试的氧化锆植入物的表面改性具有生物相容性和骨传导性。

BACKGROUND & AIMS: :Objective: To determine the effect of electro-acupuncture (EA) treatment on serum levels of interferon-γ (IFN-γ) in rats with 7,12-dimethylbenz(α)anthracene (DMBA)-induced breast tumors. Methods: Twenty five female Wistar rats were divided randomly into 5 groups: normal group (N; neither DMBA-induced nor treated with EA); control group (C; DMBA-induced only); EA 3 days : (DMBA-induced + EA for 3 days); EA 5 days: (DMBA-induced + EA for 5 days); EA 10 days: (DMBA-induced + EA for 10 days) group. Animals were acclimatized from day 1 to day 7. Subcutaneus injections of DMBA 10mg/kg BW was administered every second day, from days 7 to 35. Acupuncture was performed every second day from day 42. Rats were sacrificed on the second day after the last acupuncture, breast tumors excised and stained histological sections were analysed by light microscopy. At sacrifice, blood was extracted from the heart for measurement of serum IFN-γ by ELISA. Results: All of the DMBA-induced rats developed tumors. Electro-acupuncture significantly increased IFN-γ levels in DMBA induced rats, when compared to control group. Conclusions: Our findings suggest that EA significantly increases IFN-γ levels in DMBA-induced breast tumors.

背景与目标： ：目的：确定电针治疗对血清中干扰素-γ（IFN-γ）水平的影响
在患有7,12-二甲基苯并（α）蒽（DMBA）诱导的乳腺肿瘤的大鼠中。方法：25名女性Wistar
将大鼠随机分为5组：正常组（N；既不是DMBA诱导的，也不是用EA治疗的）。控制
组（C；仅DMBA诱导）； EA 3天：（DMBA诱导的EA 3天）； EA 5天：（DMBA诱导的EA
5天）; EA 10天：（DMBA诱导的EA 10天）组。从第1天到第7天使动物适应环境。
从第二天到第7天至第35天，皮下注射DMBA 10mg / kg体重。
从第42天起每隔第二天进行一次。最后一次针刺后第二天将大鼠处死，
通过光学显微镜分析切除的肿瘤和染色的组织学切片。牺牲时，血液被抽出
从心脏通过ELISA测定血清IFN-γ。结果：所有DMBA诱导的大鼠均出现肿瘤。
与对照组相比，电针显着增加了DMBA诱导的大鼠的IFN-γ水平。
结论：我们的发现表明，EA可以显着增加DMBA诱导的乳腺肿瘤中的IFN-γ水平。

BACKGROUND & AIMS: :Recently, an elevation in skin cholesterol level has been implicated in skin inflammation. Given the potential therapeutic effects of soy on low grade inflammatory diseases, we hypothesized that a CHOL diet could promote an inflammatory response in skin and that soy milk (SM) or fermented soy milk (F.SM) could prevent this cholesterol-induced skin inflammation. To test this hypothesis, freeze-dried SM or F.SM was provided as a protein replacement for 20% of the casein in the diets of Sprague-Dawley (SD) rats. The animals were divided into the following groups: (1) control group (CTRL), AIN76A diet without cholesterol, (2) high cholesterol (CHOL) group, AIN76A with 1% (w/w) cholesterol, (3) SM group, CHOL diet with freeze-dried SM, and (4) F.SM group, CHOL diet with F.SM. In the CHOL group, the expression levels of pro-inflammatory genes, including IL-1β, IL-1α, iNOS, and COX-2, were elevated. In comparison, the SM and F.SM groups displayed the lowered expression of IL-1β, COX-2, F4/80, and Cd68, an increase of a n-3/n-6 ratio, and a reduction in the estimated desaturase activities of delta 5 desaturase (D5D) and steaoryl CoA desaturase (SCD-1). In particular, F.SM significantly increased the proportion of dihomo-γ-linolenic acid (DGLA) in skin fatty acid (FA) composition compared with the CHOL group. Here we present evidence that SM or F.SM could alleviate the inflammatory response in the skin that is triggered by excess dietary cholesterol by reducing the expression of pro-inflammatory genes. This response could be partly associated with a decreased in macrophages in skin and/or by modulation of the skin's FA composition.

背景与目标： ：最近，皮肤胆固醇水平升高与皮肤炎症有关。考虑到大豆对低度炎症性疾病的潜在治疗作用，我们假设CHOL饮食可以促进皮肤中的炎症反应，而豆浆（SM）或发酵豆浆（F.SM）可以预防这种胆固醇诱导的皮肤炎症。为了检验这一假设，提供了冷冻干燥的SM或F.SM作为Sprague-Dawley（SD）大鼠饮食中20％酪蛋白的蛋白质替代品。将动物分为以下几组：（1）对照组（CTRL），不含胆固醇的AIN76A饮食，（2）高胆固醇（CHOL）组，含1％（w / w）胆固醇的AIN76A，（3）SM组，冻干SM的CHOL饮食，和（4）F.SM组，F.SM的CHOL饮食。在CHOL组中，促炎基因包括IL-1β，IL-1α，iNOS和COX-2的表达水平升高。相比之下，SM和F.SM组显示出IL-1β，COX-2，F4 / 80和Cd68的表达降低，n-3 / n-6比例增加以及估计的去饱和酶降低δ5去饱和酶（D5D）和硬脂酰CoA去饱和酶（SCD-1）的活性。特别是，与CHOL组相比，F.SM显着增加了皮肤脂肪酸（FA）组合物中二高-γ-亚麻酸（DGLA）的比例。在这里，我们提供的证据表明，SM或F.SM可以通过减少促炎基因的表达来减轻皮肤中由过量饮食胆固醇触发的炎症反应。该反应可能部分与皮肤巨噬细胞减少和/或通过调节皮肤的FA成分有关。

BACKGROUND & AIMS: :Menyanthes trifoliata L. is used in Swedish traditional medicine for the treatment of inflammatory diseases of the kidney, e.g. glomerulonephritis. Earlier studies have shown that MtL increases glomerular filtration rate after renal reperfusion ischemia. This activity was suggested to be PAF-inhibitory since MtL also inhibited PAF-induced exocytosis in vitro on human neutrophils (IC(50) = 0.16 mg/ml). The present study further characterizes the anti-inflammatory properties of a rhizome decoction of this plant. MtL inhibited carrageenan-induced rat paw edema (ID(50) ≈ 1.7 g/kg p.o.) and ethyl phenylpropiolate-induced rat ear edema (32% at 2.0 g/kg p.o.) in a dose-dependent manner. Further studies revealed that MtL inhibited both fMLP-induced exocytosis (IC(50) = 0.16 mg/ml) and elastase activity (IC(50) = 0.16 mg/ml). According to these results it is likely that the activity shown in the PAF-test is at least partly due to an inhibition of elastase. MtL showed only minor hemolytic properties at the concentrations used in the PAF- and fMLP-tests, suggesting that the cells in these tests are undamaged. The decoction also inhibited the biosynthesis of LTB(4) (IC(50) ≈ 0.73 mg/ml) and prostaglandins (IC(50) = 0.37 mg/ml) in vitro in a concentration-dependent way. However, at concentrations where the decoction is active in the LTB(4)-test, it also possesses hemolytic properties.

背景与目标： ：Menyanthes trifoliata L.在瑞典传统医学中用于治疗肾脏的炎症性疾病，例如肾小球肾炎。较早的研究表明，肾脏缺血再灌注后MtL可增加肾小球滤过率。该活性被认为是抑制PAF的，因为MtL还可以在体外抑制人嗜中性粒细胞的PAF诱导的胞吐作用（IC（50）= 0.16 mg / ml）。本研究进一步表征了该植物的根茎煎剂的抗炎特性。 MtL以剂量依赖的方式抑制角叉菜胶诱导的大鼠爪水肿（ID（50）≈1.7 g / kg p.o.）和苯丙酸乙酯诱导的大鼠耳水肿（2.0 g / kg p.o.时32％）。进一步的研究表明，MtL抑制fMLP诱导的胞吐作用（IC（50）= 0.16 mg / ml）和弹性蛋白酶活性（IC（50）= 0.16 mg / ml）。根据这些结果，PAF-测试中显示的活性可能至少部分是由于弹性蛋白酶的抑制。在PAF和fMLP测试中使用的浓度下，MtL仅显示出较小的溶血特性，表明这些测试中的细胞未受损。该汤还以浓度依赖的方式抑制了LTB（4）（IC（50）≈0.73 mg / ml）和前列腺素（IC（50）= 0.37 mg / ml）的生物合成。但是，在LTB（4）测试中该汤具有活性的浓度下，它也具有溶血作用。

BACKGROUND & AIMS: :Numerous lines of evidence support a relationship between intestinal inflammation and cancer. Therefore, much attention has recently been focused on the identification of natural compounds with anti-inflammatory activities as a strategy to suppress the early stages of colorectal cancer. Because cocoa is a rich source of bioactive compounds, the present study investigated its anti-inflammatory properties in a rat model of azoxymethane (AOM)-induced colon carcinogenesis and in TNF-α-stimulated Caco-2 cells. A total of forty male rats were fed with control or cocoa-enriched diets (12 %) during 8 weeks and injected with saline or AOM (20 mg/kg body weight) during the third and fourth week (n 10 rats/group). At the end of the experiment, colon samples were evaluated for markers of inflammation. The anti-inflammatory activity of a cocoa polyphenolic extract (10 μg/ml) was examined in TNF-α-stimulated Caco-2 cells, an in vitro model of experimentally induced intestinal inflammation. The signalling pathways involved, including NF-κB and the mitogen-activated protein kinase family such as c-Jun NH₂-terminal kinases (JNK), extracellular signal-regulated kinases and p38, were also evaluated. The results show that the cocoa-rich diet decreases the nuclear levels of NF-κB and the expression of pro-inflammatory enzymes such as cyclo-oxygenase-2 and inducible NO synthase induced by AOM in the colon. Additionally, the experiments in Caco-2 cells confirm that cocoa polyphenols effectively down-regulate the levels of inflammatory markers induced by TNF-α by inhibiting NF-κB translocation and JNK phosphorylation. We conclude that cocoa polyphenols suppress inflammation-related colon carcinogenesis and could be promising in the dietary prevention of intestinal inflammation and related cancer development.

背景与目标： ：大量证据支持肠道炎症与癌症之间的关系。因此，近来许多注意力集中在鉴定具有抗炎活性的天然化合物上，作为抑制结直肠癌早期阶段的策略。由于可可是生物活性化合物的丰富来源，因此本研究在由乙氧基甲烷（AOM）诱导的结肠癌发生的大鼠模型中以及在TNF-α刺激的Caco-2细胞中研究了其抗炎特性。总共40只雄性大鼠在8周内接受了对照或富含可可的饮食（12％），并在第三和第四周内注射了盐水或AOM（20 mg / kg体重）（每组10只大鼠）。在实验结束时，评估结肠样品的炎症标志物。在可诱导肠道炎症的体外模型TNF-α刺激的Caco-2细胞中检测了可可多酚提取物（10μg/ ml）的抗炎活性。还评估了涉及的信号通路，包括NF-κB和丝裂原活化的蛋白激酶家族，例如c-Jun NH 2末端激酶（JNK），细胞外信号调节激酶和p38。结果表明，富含可可的饮食降低了结肠中NF-κB的核水平，降低了AOM诱导的促炎性酶（如环氧化酶2和可诱导的NO合酶）的表达。此外，在Caco-2细胞中进行的实验证实，可可多酚通过抑制NF-κB易位和JNK磷酸化，有效下调TNF-α诱导的炎症标志物的水平。我们得出的结论是，可可多酚抑制炎症相关的结肠癌发生，并且在饮食预防肠道炎症和相关的癌症发展中可能很有希望。