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Mild intrauterine hypoperfusion(MIUH) is a serious pathological event that affects the growth and development of fetuses and offspring. MIUH can lead to growth restriction, low birth weight, neurodevelopmental disorders, and other adverse clinical outcomes. To study the effects of MIUH on learning and memory function in offspring, a model of MIUH was established by placing a coil(length 2.5 mm, diameter 0.24 mm) on the uterine artery and ovarian uterine artery of Sprague-Dawley rats in the second trimester of pregnancy(day 17). Next, 120 mg/kg lithium chloride(the MIUH + Li group) or normal saline(the MIUH group) was injected intraperitoneally into these rats. In addition, 120 mg/kg lithium chloride(the Li group) or normal saline(the SHAM group) was injected intraperitoneally into pregnant rats without coil placement. The Morris water maze was used to detect changes in learning and memory ability in the offspring at 4 weeks after birth. In the MIUH group, the escape latency and journey length before reaching the platform were both increased, and the number of times that the platform was crossed and the activity time in the target quadrant within 90 seconds were both decreased compared with the SHAM group. Immunofluorescence double staining and western blot assays demonstrated that hippocampal nestin and Ki67(both cell-proliferation-related proteins) expression was significantly downregulated in the MIUH group compared with the SHAM group. Furthermore, western blot assays were conducted to investigate changes in related signaling pathway proteins in the brains of offspring rats, and revealed that glycogen synthase kinase 3β(GSK3β) expression was upregulated and β-catenin expression was downregulated in the MIUH group compared with the SHAM group. In addition, compared with the MIUH group, the expression levels of p-GSK3β and β-catenin were upregulated in the MIUH + Li group. These results suggest that MIUH may affect learning and memory function in rat offspring by regulating the GSK3β signaling pathway. The experimental procedures were approved by Animal Ethics Committee of Shengjing Hospital of China Medical University(approval No. 2018 PS07 K) in June 2018. 相似文献
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The study was to detect the role of GDNF, PGP9.5 (a neuronal marker), and GFAP (EGCs’ marker) in the mechanism of non-steroidal anti-inflammatory drugs (NSAIDs) related to intestinal injury and to clarify the protective effect of berberine in the treatment of NSAID-induced small intestinal disease. Forty male SD rats were divided randomly into five groups (A–E): Group A: control group; Group B: model group received diclofenac sodium 7.5 mg/(kg*day) for 5 days; Group C–E: berberine low, medium and high dose groups were treated by 7.5 mg/(kg*day) diclofenac sodium for 5 days then received berberine 25 mg/(kg*day), 50 mg/(kg*day), and 75 mg/(kg*day), respectively, between the sixth and eighth day. Intestinal mucosa was taken on the ninth day to observe the general, histological injuries, and to measure the intestinal epithelial thickness. Then, immunohistochemistry was performed to detect the expression of PGP9.5 and GFAP, and Western blot was performed to detect GDNF expression. The histological score and the general score in the model group were, respectively, 5.75 ± 1.04 and 4.83 ± 0.92. Scores in berberine medium and high berberine group were lower compared with the model group (P < 0.05). The intestinal epithelial thickness in the model group was lower than in the control group and the berberine groups (P < 0.05). PGP9.5, GFAP, and GDNF content in the model group and the three berberine groups were significantly lower than in the control groups (P < 0.05). PGP9.5, GFAP, and GDNF content in the control group and the three berberine groups were higher compared with the model groups (P < 0.05). Berberine can protect the intestinal mucosa of NSAID users, and the mechanism is associated with the reparation of the enteric nervous system via upregulating the expression of PGP9.5, GFAP, and GDNF. 相似文献
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目的探讨颈椎手法牵引复位联合舒适护理在颈椎病患者中的应用效果。方法选择2017年8月-2019年6月收治的80例颈椎病患者,采用随机数字表法分为2组,各40例。在颈椎手法牵引复位的基础上,对照组采用常规护理,观察组采用舒适护理,比较2组临床疗效、生活质量。结果干预后,较对照组相比,观察组总有效率高、WHOQOL-BREF各维度评分高,差异有统计学意义(P<0.05)。结论颈椎病患者采用颈椎手法牵引复位联合舒适护理可提高治疗效果,改善患者生活质量。 相似文献
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目的 探索电子顺磁波谱(electron paramagnetic resonance,EPR)技术检测红参清除自由基活性的适合产生体系,并研究红参对羟自由基(?OH)的清除作用及其物质基础。方法 采用电子顺磁共振波谱仪检测不同浓度的红参提取液对?OH的体外清除作用,并用液质联用技术(LC-MS)分析红参中的主要皂苷成分,然后研究这些人参皂苷成分对?OH的清除作用。结果 确定了羟自由基的生成体系为:Fe2+ 0.1 mmol?L-1、H2O2 500 mmol?L-1、DMPO 225 mmol?L-1;不同浓度的红参提取液对?OH具有明显的清除作用,且其清除?OH的效力与浓度成正相关;LC-MS分析显示该红参提取液中主要含有Rh1、Rf、Rb3、F1、F2、Rg3、Rg5等成分,其中人参皂苷Rg5的清除自由基活性最强。结论 本研究建立了用EPR技术研究红参清除自由基活性的适合产生体系,红参具有明显的清除?OH的能力,且人参皂苷Rg5是其清除自由基的活性成分之一,确定了红参抗自由基的主要物质基础,为红参及人参皂苷Rg5的开发、应用提供了科学依据和理论基础。 相似文献
79.
目的:观察脂多糖(lipopolysaccharide,LPS)诱导肺成纤维细胞及肺组织有氧糖酵解关键酶6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶3(6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3,PFKFB3)表达及其与有氧糖酵解的关系,探讨在LPS诱导肺纤维化过程中肺成纤维细胞和肺组织有氧糖酵解的潜在机制。方法:将人胚肺成纤维细胞MRC-5细胞系采用随机数字表法分为PBS对照组(PBS组)和LPS组(每组3孔),Western blot检测LPS刺激细胞6h后PFKFB3表达情况,同时免疫荧光显示PFKFB3在细胞内的定位情况;于LPS刺激后48 h采用海马细胞能量代谢仪检测细胞耗氧率(oxygen consumption rate,OCR)和产酸率(extracellular acidification rate,ECAR),并采用比色法检测有氧糖酵解产物乳酸产生情况,同时Western blot检测LPS刺激48 h后Ⅰ型胶原蛋白合成情况。将24只C57BL/6小鼠按随机数字表法分为生理盐水对照组(C组)、LPS组(L组),每组12只,L组、C组连续5d分别腹腔注射5 mg/kg LPS、等容量生理盐水;每组各6只于造模后第7天无痛处死小鼠,取血浆和肺组织,Western blot和免疫荧光检测各组肺组织中PFKFB3表达情况,比色法检测各组小鼠血浆中乳酸的含量;剩余小鼠于造模后第28天取肺组织,一侧肺通过Western blot检测肺组织Ⅰ型胶原蛋白合成情况,另一侧肺做石蜡切片进行病理学检测。结果:与PBS组比较,LPS刺激细胞6h后PFKFB3表达明显升高(P<0.05);LPS刺激细胞48 h后,与PBS组比较,LPS组细胞耗氧率降低、产酸率增加,代谢产物乳酸含量明显升高(P<0.05),同时细胞Ⅰ型胶原蛋白合成显著增加(P<0.05)。与C组比较,L组小鼠腹腔注射LPS 7 d后肺组织中PFKFB3表达明显升高(P<0.05),血浆乳酸含量明显升高(P<0.05);LPS注射28 d后,L组小鼠Ⅰ型胶原蛋白表达明显升高(P<0.05),肺组织出现明显纤维化。结论:在LPS诱导的肺纤维化过程中,LPS可诱导肺成纤维细胞和肺组织中PFKFB3蛋白表达,该过程与其有氧糖酵解过程相关,PFKFB3的表达上调可能是LPS诱导肺成纤维细胞和肺组织有氧糖酵解和肺纤维化的关键环节。 相似文献
80.
目的 探讨脑白质疏松与老年急性脑梗死静脉溶栓患者症状性颅内出血(symptomatic intracranial
hemorrhage,sICH)及功能预后的关系。
方法 纳入2016年1月1日-2018年12月31日连续就诊于北京怀柔医院的老年急性脑梗死静脉溶栓
患者。根据入院头颅CT,采用改良Van Swieten量表进行脑白质疏松分级。应用多因素Logistic回归模型,
分析脑白质疏松与溶栓后24 h sICH和3个月不良功能预后(mRS>2分)的关系。
结果 共纳入125例患者,平均年龄73.2±8.4岁,男性84例(67.2%),有脑白质疏松82例(65.6%)。
有脑白质疏松、无脑白质疏松患者溶栓后24 h sICH发生率分别为12.2%(10/82)、4.7%(2/43),
P =0.298;3个月不良功能预后比例分别为70.7%(58/82)、34.9%(15/43),P <0.001。多因素
Logistic回归分析显示,脑白质疏松与老年急性脑梗死静脉溶栓患者24 h sICH不相关(OR 0.320,
95%CI 0.056~1.846,P =0.203);与3个月不良功能预后独立相关(OR 4.392,95%CI 1.514~12.744,
P =0.006)。
结论 脑白质疏松症与老年急性脑梗死静脉溶栓患者sICH不相关,但与静脉溶栓治疗后3个月不良
功能预后独立相关。 相似文献