排序方式： 共有34条查询结果，搜索用时 15 毫秒
1.
目的:在康脑液方剂干预下观察皮质区内源性神经细胞干细胞因子(SCF)mRNA在大鼠脑缺血再灌注损伤后不同时间的表达情况。方法:成年SD大鼠,以线栓法建立大脑中动脉缺血再灌注模型,随机分为模型组、药物干预组和假手术组。原位杂交技术检测脑缺血1.5h再灌注1～14d后,脑皮质区SCFmRNA表达情况。结果:脑缺血再灌注后,药物干预组、模型组SCFmRNA的表达在皮质区均明显高于假手术组,于第7天达高峰,第14天下降。结论:药物干预后脑缺血再灌注脑皮质区SCFmRNA表达在不同时间点与模型组具备相同的表达规律,两组SCFmRNA的表达无显著性差异。 相似文献
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蜂王浆对大鼠力竭运动能力影响的实验研究 总被引：7，自引：0，他引：7
研究目的：探讨服用蜂王浆的大鼠，作力竭运动时，减轻和防止自由基对机体组织的损伤和抗疲劳作用。研究方法：灌喂蜂王浆的大鼠为试验组与对照组比较，测试二组在力竭运动时体重、运动能力、线粒体丙二醛（MDA）、超氧化物歧化酶（SOD）、血浆PH值，血乳酸、血清总钙ATP的合成能力以及肝、肌糖原的变化。研究结果：实验组与对照组比较体重明显增加，运动能力显著提高，MDA降低明显，SOD活性显著增高，ATP和PH值相应提高，血乳酸和血清总钙较低，肝、肌糖原明显增多。蜂王浆作为一种有效的体能恢复剂在推广和利用上有广泛的前景。 相似文献
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选用192只28±2d实验用清洁级SD大鼠,分为6组,每组32只,雌雄各半,分别饮用添加硼0、40、80、160、320和640mg/L的蒸馏水,试验期60d,分别于试验第30d(65日龄)和60d(95日龄)每组随机取鼠16只,雌雄各8只,10%水合氯醛腹腔麻醉,立即解剖取胸腺,称重,制作石蜡切片,HE染色,光镜观察并显微摄影.结果显示:与对照组相比较,65日龄试验Ⅲ～Ⅴ组雄鼠和试验Ⅴ组雌鼠胸腺质量显著或极显著降低(P＜0.05或P＜0.01);95日龄试验Ⅰ组雄鼠胸腺质量显著升高(P＜0.05),试验Ⅴ组雄鼠和雌鼠显著或极显著降低(P＜0.05或P＜0.01).65日龄和95日龄试验Ⅴ组雄鼠和雌鼠胸腺器官指数显著低于对照组(P＜0.05);试验Ⅰ、Ⅱ组胸腺结构表现较明显促进作用;试验Ⅲ、Ⅳ组胸腺结构呈现一定的退化迹象;试验Ⅴ组胸腺结构退化现象明显,实质内淋巴细胞数量明显减少.试验结果表明,饮水添加40、80mg/L硼对大鼠胸腺发育及其组织结构有较明显促进和改善作用;添加160、320mg/L硼对胸腺发育有一定不良影响;添加640mg/L硼对大鼠胸腺发育则有明显的抑制甚至毒性作用. 相似文献
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目的利用1.5T质子磁共振波谱（^1H-MRS）监测活体帕金森病大鼠模型骨髓间充质干细胞（mesenchymal stem cells,MSCs）移植治疗前后纹状体区的神经代谢变化,以探讨1．5T磁共振波谱分析在评价MSCs移植术疗效中的应用价值。方法30只正常大鼠,以6-羟基多巴胺（6-OHDA）单侧（右侧）损毁制备偏侧帕金森病模型。在活体状态下,分别于造模后3周、MSEs移植后4周及8周应用Philips1．5T临床型磁共振仪扫描,对双侧纹状体区进行^1H—MRS采集,分析该区N-乙酰天门冬氨酸／肌酸（NAA／Cr）、胆碱／肌酸（Cho／Cr）比值变化,同时对大鼠进行行为学检测。利用黑质酪氨酸羟化酶免疫组织化学染色对黑质致密部（SNc）神经元进行定量分析。结果MSCs移植后8周组（C组）大鼠损毁侧（右侧）NAA／Cr比值与未处理组（A组）和MSCs移植后4周组（B组）相比明显升高（P〈0．05）;B,C组损毁侧Cho／Cr比值较A组明显降低（P〈0．05）,且分别明显低于其对侧（P均〈0．05）。B,C组旋转圈数分别较A组低（P均〈0．05）正组旋转圈数较B组显著降低（p〈0．05）。三组损毁侧SNCTH阳性细胞生存率无显著差异（P均〉0．05）。结论1．5T磁共振波谱可以作为一种活体无创性检测方法,对帕金森病大鼠模型纹状体区MSCs细胞移植疗效进行动态监测而作出有价值的评价。 相似文献
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力竭性运动对鼠和人的影响的研究进展 总被引：1，自引：0，他引：1
运用文献资料法，阐述力竭性运动对鼠和人的心脏、骨骼肌、消化系统、肾脏和血细胞等产生的影响，并分析产生影响的主要原因． 相似文献
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目的：研究自发性高血压大鼠（SHR）膈肌功能的变化。方法：大鼠随机分成两组，SHR组和Wistar大鼠组，各8只，应用体外灌流大鼠膈肌条的方法，测量张力一频率曲线，疲劳指数的变化，同时测定膈肌组织中的超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮合酶（NOS）活性（总NOS和iN0s）和NO含量的变化。结果：与对照组相比，SHR组大鼠膈肌张力-频率曲线右移，疲劳指数下降明显（P〈0．01），组织中SOD、总NOS活性和NO含量显著降低（P〈0．01），iNOS、MDA含量显著增加（P＜0．01）。结论：自发性高血压大鼠膈肌功能受到损伤。 相似文献
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目的研究不同年龄自发性高血压大鼠血管平滑肌Ca2+/CaM-PP活性变化.方法应用酶活性测定方法,对12周、16周SHR大鼠和Wistar大鼠的A、MA、CA血管平滑肌Ca2+/CaM-PP进行活性比较.结果Wistar大鼠随年龄增长,Ca2+/CaM-PP活性呈上升趋势,而SHR鼠其阻力血管该酶活性降低,但随年龄变化不明显.结论①自发性高血压使阻力血管平滑肌Ca2+/CaM-PP下降,但12周与16周间无显著差异.②不同种鼠血管平滑肌该酶活性变化不同. 相似文献
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Fabrice Tranchida Léopold Tchiakpe Zo Rakotoniaina Valérie Deyris Olivier Ravion Abel Hiol 《Journal of Zhejiang University. Science. B》2012,13(4):307-317
As the consumption of fructose and saturated fatty acids (FAs) has greatly increased in western diets and is linked with an increased risk of metabolic syndrome, the aim of this study was to investigate the effects of a moderate (10 weeks) and a prolonged (30 weeks) high fructose and saturated fatty acid (HFS) diet on plasma FA composition in rats. The effects of a few weeks of HFS diet had already been described, but in this paper we tried to establish whether these effects persist or if they are modified after 10 or 30 weeks. We hypothesized that the plasma FA profile would be altered between 10 and 30 weeks of the HFS diet. Rats fed with either the HFS or a standard diet were tested after 10 weeks and again after 30 weeks. After 10 weeks of feeding, HFS-fed rats developed the metabolic syndrome, as manifested by an increase in fasting insulinemia, total cholesterol and triglyceride levels, as well as by impaired glucose tolerance. Furthermore, the plasma FA profile of the HFS group showed higher proportions of monounsaturated FAs like palmitoleic acid [16:1(n-7)] and oleic acid [18:1(n-9)], whereas the proportions of some polyunsaturated n-6 FAs, such as linoleic acid [18:2(n-6)] and arachidonic acid [20:4(n-6)], were lower than those in the control group. After 30 weeks of the HFS diet, we observed changes mainly in the levels of 16:1(n-7) (decreased) and 20:4(n-6) (increased). Together, our results suggest that an HFS diet could lead to an adaptive response of the plasma FA profile over time, in association with the development of the metabolic syndrome. 相似文献
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To investigate the inhibiting effect of β-Aescin on nuclear factor-κB (NF-κB) activation and the expression of tumor necrosis factor-α (TNF-α) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) β-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). β-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6h, 24 h and 3 d respectively after trauma in four groups. NF-κB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-α protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-κB activation, the levels of TNF-α protein and the water content of rat brain were significantly increased (P＜0.01) following TBI in rats. Compared with Group B, NF-κB activation (P＜0.01), the levels of TNF-α protein (P＜0.01) and the water content of brain (P＜0.05) began to decrease obviously after injury in Groups C and D.β-Aescin could dramatically inhibit NF-κB activation and the expression of TNF-α protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which β-Aescin attenuates traumatic brain edema. 相似文献
10.
BackgroundCancer is a life-threatening disease that affects approximately 18 million individuals worldwide. Breast cancer is the most common female neoplasm globally with more than 276,480 new cases of invasive breast cancer expected to be diagnosed in women in the U.S. alone in 2020. Genetic and epigenetic factors play role in the carcinogenesis and progression of this disease. In this study, MCF-7 adenocarcinoma cells were transfected with CRISPR/Cas9 plasmid to either knock out CDK11 or to activate CDH1. Treated cells were allografted into the mammary glands of female rats (150–190 g, 6–8 weeks) to evaluate the capability of these cells to control cancer progression and metastasis.ResultsqPCR data revealed a significant downregulation of CDK11 and upregulation of CDH1. Cell cycle analysis and apoptosis assays indicated the knockout of CDK11 and simultaneous activation of CDH1 resulted in cell cycle arrest at G2/M phase and accumulation of cells at G2. Meanwhile, the percentage of cells that underwent late apoptosis increased in both genome editing hits. Histopathological sectioning data indicated that untransfected MCF-7 cells were capable of developing tumors in the mammary gland and initiation g angiogenesis. Transfected cells significantly restricted cancer cell infiltration/invasion by minimally localizing tumors and inhibiting angiogenesis.ConclusionsAlthough further investigation is needed, the present data indicate the potentiality of using CRISPR/Cas9-based therapy as a promising approach to treat breast cancer. Impact: these data indicate targeting cancer-related genes via any genome editing tool might represent a novel approach to combat cancer.How to cite: Al-Mulhim F, Alqosaibi AI, Al-Muhnna A, et al. CRISPR/Cas9-mediated activation of CDH1 suppresses metastasis of breast cancer in rats. Electron J Biotechnol 2021;53. https://doi.org/10.1016/j.ejbt.2021.06.002 相似文献