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FoxO3a inhibits the expression of neuropeptide W in neuronal cells and rat hypothalamus and its effect on the hypothalamic-pituitary-adrenal(HPA) axis

FoxO3a inhibits the expression of neuropeptide W in neuronal...

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世界中医药学会联合会老年医学专业委员会2021年学术年...

作者： Chao Yang Wenshu Zhou xingan xing Wenhua Zheng Centre of Reproduction Development and Aging Institute of Translational MedicineFaculty of Health Sciences University of Macau

Forkhead box O3(FoxO3a), a transcription factor in forkhead family, is associated with the regulation of cell proliferation, metabolism, differentiation and apoptosis. However, whether FoxO3a is involved in the regulation of glucocorticoids induced-hypothalamic-pituitary-adrenal(HPA) dysfunction is not well known. Our current results demonstrated that dexamethasone(DEX) could upregulate the expression of FoxO3a in PC12 and hypothalamic neuronal cultures while downregulate the expression level of neuropeptide W(NPW), dna this process could be blocked by GR2 antagonist. Furthermore, DEX inhibited the phosphorylation of Akt and FoxO3a, but did not inhibit the phosphorylation of ERK1/2, resulting with FoxO3a nuclear localization. We also found that the overexpression of FoxO3a could inhibit NPW expression, while the FoxO3a knockdown by siRNA had the opposite effect, as the regulatory region of NPW promoter contains multiple FoxO3a binding sites, the FoxO3a inhibited NPW’s transcriptional activity by bonding to these sites. Additionally, in the rat model, long-term use of corticosteroids could reduce animals’ body weight and sucrose consumption and cause stress-depression like behavior. Moreover corticosterone treatment caused a significant increase in FoxO3a levels, while the expression of NPW protein decreased in the hypothalamus. Meanwhile, FoxO3a and NPW were co-located in the hypothalamus proved by using immunofluorescent double labeling. In summary, these results indicate that NPW is a new direct downstream target gene of FoxO3a. FoxO3a inhibited the transcription of NPW and regulated glucocorticoids-induced HPA dysfunction by directly regulating the expression of NPW. Therefore, the current findings suggest that FoxO3a and NPW may be potential therapeutic targets for endocrine and mental disorders.

关键词： Glucocorticoids Neuropeptide W （NPW） FoxO3a HPA axis dysfunction Hypothalamus

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Artemisinin reverses glucocorticoid-induced injury in bone marrow derived mesenchymal stem cells through regulation of ERK1/2-CREB signaling pathway

Artemisinin reverses glucocorticoid-induced injury in bone m...

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世界中医药学会联合会老年医学专业委员会2021年学术年...

作者： xingan xing Jiankang Fang Marta Silva Ruohong Lin Wenhua Zheng Centre of Reproduction Development and Aging Institute of Translational MedicineMoE Frontiers Science Center for Precision Oncology Faculty of Health SciencesUniversity of Macau

Glucocorticoids are the most common cause of secondary osteoporosis, which affects both women(pre-and post-menopausal) and men. In cases of prolonged treatment, glucocorticoids promote the loss and inactivation of the differentiational function of bone marrow mesenchymal stromal cells(BMSCs), risking the development of skeletal system diseases such as osteoporosis. This study reports for the first time the protective effect of the antimalarial artemisinin against glucocorticoid-induced insults on primary cultured rat BMSC. At clinically relevant concentrations, artemisinin treatment improved BMSCs survival by promoting a decline of reactive oxygen specias(ROS) production that correlated with the decrease of Caspase 3 activation, LDH release, Δψm loss and apoptosis induced by dexamethasone(DEXA). Additionally, artemisinin improved the osteogenic differentiation of DEXA-damaged cells. DEXA inhibited extracellular-signal-regulated kinase 1/2(ERK1/2) and c AMP response element binding protein(CREB) phosphorylation, and artemisinin treatment promoted their activation in a concentration-dependent manner. PD98059, the specific inhibitor of the ERK1/2 pathway, blocked ERK1/2 phosphorylation and artemisinin protection. Similarly, siCREB attenuated the protective effect of artemisinin, strongly suggesting the involvement of the ERK1/2-CREB pathway in the protective action of artemisinin against DEXA damage in BMSCs.

关键词： Artemisinin Dexamethasone BMSC ERK pathway

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Artemisia annua extracts improve the cognitive deficits and reverse the pathological changes of Alzheimer's disease via the Hippo pathway

Artemisia annua extracts improve the cognitive deficits and ...

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世界中医药学会联合会老年医学专业委员会2021年学术年...

作者： WenShu Zhou Yang Chao Marta Silva xingan xing YiTian Chen WenHua Zheng Center of Reproduction Development & Aging Faculty of Health SciencesUniversity of Macau Institute of Translation Medicine Faculty of Health Sciences University of Macau

Alzheimer’s disease(AD) is a chronic neurodegenerative disease characterized by cognitive deficits such as the loss of memory of recent events. The major pathological changes of AD are extracellular amyloid-β(Aβ) plaques and intracellular neurofibrillary tangles(NFTs) composed of hyperphosphorylated microtubule-associated tau protein and lot of neuronal death. So far, there is no effective drug for the treatment of AD and the search for new effective therapies has become the major focus. In this study, we describe the potential therapeutic effect on AD of a water solvable artemisia annua extract(Ex1) in vivo and in vitro. Our in vitro studies revealed that Ex1 significantly reversed Aβ1-42-induced increase of ROS levels, caspase-3 activity, and neuronal cell apoptosis. Western blot analysis showed that Ex1 alleviated Aβ1-42-induced inflammation and the phosphorylation of Tau. It also stimulated the activation of YAP/TAZ signaling pathway in PC12 cells in a time and concentration-dependent manner indicating the involvement of this pathway in the effect of Ex1. Consistent with this hypothesis, inhibition of the YAP/TAZ signaling pathway by its specific inhibitor or siRNA reduced the neuroprotective effect of the Ex1. More importantly, oral administration of the Ex1 to AD 3xTg mice significantly improved the cognitive deficits, reduced Aβ accumulation, hyper-tau-phosphorylation and the release of inflammatory factor and apoptosis in AD mice. Additionally, Ex1 promoted the survival and proliferation of neural progenitor cells(NPs), increased the expression of synaptic proteins and neuronal cell survival. The extracts also stimulated the activation of YAP/TAZ signaling pathway in 3xTg AD mice like it does in previous studies in PC12 cells. Taken together, these findings revealed that Ex1 is able to relief AD symptoms and to reverse the pathological changes of AD in vitro and in vivo via the activation of the YAP/TAZ pathway. Our findings also suggest that Ex1 may be a new multi-targets anti-AD drug that can be used in

关键词： Alzheimer’s disease Artemisia annua extracts Neuronal apoptosis AD-type pathologies 3xTg mice

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高脂饮食和丁酸钠干预对大鼠十二指肠线粒体能量代谢和肠钙吸收的影响

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食品科学 2020年第1期41卷 147-156页

作者：马淑华唐雪张凯孙勇娟李颖瑞幸新干江南大学食品学院食品营养与功能食品工程技术研究中心

目的:探讨丁酸钠(sodium butyrate,NaB)对肥胖易感(obesity prone,OP)和肥胖抵抗(obesity resistant,OR)大鼠十二指肠线粒体能量代谢和肠钙吸收的影响。方法:将70只SD雄性大鼠随机分为5组:正常饮食组(CON)、肥胖易感组(OP)、肥胖易感Na... 详细信息

目的:探讨丁酸钠(sodium butyrate,NaB)对肥胖易感(obesity prone,OP)和肥胖抵抗(obesity resistant,OR)大鼠十二指肠线粒体能量代谢和肠钙吸收的影响。方法:将70只SD雄性大鼠随机分为5组:正常饮食组(CON)、肥胖易感组(OP)、肥胖易感NaB干预组(OP+4%NaB)、肥胖抵抗组(OR)及肥胖抵抗NaB干预组(OR+4%NaB)。每周监测大鼠体质量增加量和采食量,20周实验结束,采样分析其十二指肠氧化还原状态相关指标、线粒体抗氧化酶活力、能量代谢以及钙吸收和血钙稳态相关指标;采用实时荧光定量聚合酶链式反应对十二指肠抗氧化通路、钙离子转运相关基因表达进行分析;用Western blot对重要抗氧化蛋白表达水平进行分析。结果:与OP组相比,OP+4%NaB组大鼠体质量增加量显著降低(P0.05)。与OR组相比,OR+4%NaB组大鼠钙平衡实验和血液钙稳态及钙离子转运相关指标也无显著性差异(P>0.05)。结论:Na B干预可提高OP和OR组大鼠十二指肠抗氧化能力,减少ROS产生,维护线粒体氧化还原稳态,增加OP大鼠肠钙贮留水平和钙离子转运能力,且干预效果在不同肥胖表型大鼠中存在差异,对OP表型效果最好。

关键词：线粒体丁酸钠抗氧化氧化应激肥胖易感

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Artemisinin inhibits the migration and invasion in Uveal Melanoma via inhibition of the PI3K/AKT/mTOR signaling pathway

Artemisinin inhibits the migration and invasion in Uveal Mel...

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世界中医药学会联合会老年医学专业委员会2021年学术年...

作者： Mohd Farhan Marta Silva xing xingan Zhiwei Zhou Wenhua Zheng Cancer Center and Center of Reproduction Development & Aging Faculty of Health Sciences University of Macau Taipa Macau SAR China and Institute of Translation Medicine Faculty of Health Sciences University of Macau

Uveal melanoma is the most common primary ocular neoplasm in adults, with many patients ending up developing liver metastasis and facing a significant reduction of their life expectancy due to the lack of efficient treatments able to prevent or reduce their occurrence. Artemisinin is an anti-malarial drug that has been widely used in the clinic and whose anticancer properties have also been described. Its reported safety, affordability and ability to reach the ocular tissues point it has a potential therapeutic agent against uveal melanoma. In the present study, we found that a sub-anti-malaria dosage of artemisinin significantly attenuated the migration and invasion potential of uveal melanoma cells, in a concentration-dependent manner. Assessment of the mechanisms underlying artemisinin anticancer action, revealed that its use dramatically reduced the phosphorylation of PI3K, AKT and mTOR in UM cells. Further inhibition of PI3K signaling, using LY294002, or of mTOR, by rapamycin, blocked the migration and invasion of UM cells similarly to artemisinin. In contrast, AKT or mTOR activation(Sc79 or MHY1485, respectively), attenuated the inhibitory effect of artemisinin on the migration and invasion abilities of UM cells, further validating that artemisinin’ anticancer effect is likely to be mediated via inhibition of the PI3K/AKT/mTOR pathway. Artemisinin also induced mitochondrial membrane potential loss and apoptosis of UM cells, having no significant toxic effect in normal retinal neuronal cells RGC-5 and epithelial cells D407. These findings and the fact that the clinical dosage of artemisinin is very safe, strongly suggest that artemisinin is a safe drug for the prevention and treatment of uveal melanomas.

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IGF-1 induced migration and invasion of Uveal melanoma cell is mediated by FoxO3a transcriptional factor

IGF-1 induced migration and invasion of Uveal melanoma cell ...

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世界中医药学会联合会老年医学专业委员会2021年学术年...

作者： Shan Zeng Mohd Farhan Yan Fengxia Liao Rifang xing xingan Zhiwei Zhou Wenhua Zheng Cancer Center and Center of Reproduction Development & Aging Faculty of Health Sciences University of Macau Institute of Translation Medicine Faculty of Health Sciences University of Macau The School of Pharmaceutical Sciences Sun Yat-Sen University

In adults, Uveal melanoma(UM) is common primary intraocular malignancy with high mortality rate due to liver metastasis. Epidemiology and pathogenesis of liver metastasis in UM are not elucidated and no effective therapy is available for UM. IGF-1 is a growth factor involved in cell proliferation, malignant transformation and inhibition of apoptosis. Earlier, IGF-1 receptor was found to be highly expressed in UM, which is related to tumor prognosis. FoxO3a is a Forkhead box O(FOXO) transcription factor and a downstream target of IGF-1R/PI3K/Akt pathway involved in a number of pathophysiological processes including cancer. However, the role of FoxO3a in UM is unknown. In this study, we investigated the involvement of FoxO3a in migration and invasion of UM. Western blot analysis showed that IGF-1 led to activation of Akt and concomitant phosphorylation of FoxO3a which is associated with its translocation into the cytoplasm from the nucleus and its functional inhibition led to the inhibition of expression of Bim and p27, but an increase in the expression of Cyclin D1. The effects of IGF-1 on UM cells were reversed by LY294002 or Akt siRNA, and overexpression of FoxO3a also attenuated basal invasion and migration of UM. Taken altogether, these result suggest that inhibition of FoxO3a by IGF-1 via PI3K/Akt pathway has an important role in IGF-1 induced proliferation and invasion of UM. These findings also suggest that FoxO3a and IGF signaling may represent a valid target for investigating the development of new strategies for treatment and prevention of pathology of UM.

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晶体中声子和光子的区别与联系

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陕西师范大学学报（自然科学版） 2004年第S1期32卷 78-80页

作者：侯清玉包立平兴安职业技术学院兴安盟通信公司内蒙古乌兰浩特137400

对光子和声子的特点、光子和声子产生的机制、晶体中光子和电子相互作用规律及声子与电子相互作用规律,进行了全面的类比区别.并且利用晶体中光子和声子相互作用的规律,阐明了光子和声子的联系.

关键词：晶体光子声子

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大兴安岭中段晚三叠世四分组效应花岗岩的厘定及其地质意义

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岩石学报 2016年第9期32卷 2793-2806页

作者：李世超李永飞王兴安朱凯吉林大学地球科学学院长春130061 中国地质调查局沈阳地质调查中心沈阳110034 东北师范大学地理科学学院长春130024

布敦化岩体位于中亚造山带东段大兴安岭地区的科尔沁右翼中旗,该岩体由中细粒二云母花岗岩和斑状中细粒白云母花岗岩组成。LA-MC-ICP-MS锆石U-Pb同位素年龄测试显示布敦化岩体形成于晚三叠世早期。地球化学分析表明,该岩体为弱过铝质-... 详细信息

布敦化岩体位于中亚造山带东段大兴安岭地区的科尔沁右翼中旗,该岩体由中细粒二云母花岗岩和斑状中细粒白云母花岗岩组成。LA-MC-ICP-MS锆石U-Pb同位素年龄测试显示布敦化岩体形成于晚三叠世早期。地球化学分析表明,该岩体为弱过铝质-过铝质、高钾钙碱性系列,主量元素表现出高硅（73.73%-78.33%）、富碱（Na2O＋K2O=7.07%-9.06%）、低钙（Ca O=0.01%-0.87%）、贫镁（Mg O=0.12%-0.52%）的特征;稀土元素具有明显的Eu负异常和M型四分组效应配分型式。岩石学和地球化学特征显示布敦化岩体为高分异I型花岗岩。Lu-Hf同位素研究显示其εHf（t）值为7.0-12.4,二阶段Hf模式年龄（tDM2）为812-473Ma。结合邻区晚三叠世地质资料可知,布敦化岩体是在古亚洲洋闭合造山后伸展的构造背景下产生的,是晚元古代-早古生代地壳物质熔融的产物。布敦化地区的四分组效应花岗岩的稀土元素总量高、岩浆侵位后经历了强烈的分异演化,暗示布敦化地区可能具有较好的稀有金属矿的找矿前景。

关键词：布敦化四分组效应稀有金属矿晚三叠世大兴安岭

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大兴安岭中部柴河地区钾长花岗岩的成因及构造背景:岩石地球化学、锆石U-Pb同位素年代学的制约

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岩石学报 2012年第8期28卷 2647-2655页

作者：王兴安徐仲元刘正宏朱凯吉林大学地球科学学院长春130061

对大兴安岭中部柴河林场地区钾长花岗岩进行了系统的地球化学及锆石U-Pb同位素年代学研究,并对其岩石成因及构造意义进行讨论。研究结果表明,柴河林场地区钾长花岗岩中锆石具有典型的岩浆振荡生长环带和较高的Th/U比值(0.44～1.42),反... 详细信息

对大兴安岭中部柴河林场地区钾长花岗岩进行了系统的地球化学及锆石U-Pb同位素年代学研究,并对其岩石成因及构造意义进行讨论。研究结果表明,柴河林场地区钾长花岗岩中锆石具有典型的岩浆振荡生长环带和较高的Th/U比值(0.44～1.42),反映了岩浆成因特征。LA-ICP-MS锆石U-Pb定年结果为133±3Ma。岩石具有富硅、稀土元素含量较高、相对富集轻稀土元素亏损重稀土元素的特征,Eu负异常较为明显,稀土元素配分图解具有右斜"V"字型的特征,并相对富集高场强元素和大离子亲石元素。以上特征表明,柴河林场地区钾长花岗岩为铝质A型花岗岩,是地壳岩石部分熔融的产物,具有典型A1型(裂谷或板内)花岗岩的特征,代表了伸展的构造环境。

关键词：大兴安岭钾长花岗岩年代学 A型花岗岩伸展构造

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远程护理干预对手指屈肌腱断裂吻合术后患者遵医行为的影响

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护士进修杂志 2014年第4期29卷 317-319页

作者：余鑫张晓杰单欣刚李岩吉林大学第一医院手足外科吉林长春130031

目的探讨远程护理干预对手指屈肌腱断裂修复术后患者遵医行为的影响。方法将76例门诊行手指屈肌腱断裂修复术患者随机分为对照组与观察组,每组38例,对照组患者仅术后进行手指屈肌腱修复后的健康教育;观察组患者离院后,根据远程护理计划... 详细信息

目的探讨远程护理干预对手指屈肌腱断裂修复术后患者遵医行为的影响。方法将76例门诊行手指屈肌腱断裂修复术患者随机分为对照组与观察组,每组38例,对照组患者仅术后进行手指屈肌腱修复后的健康教育;观察组患者离院后,根据远程护理计划流程进行持续护理干预,分别于术后、第一次换药、拆线时及拆除石膏时发放调查问卷,评价两组患者在遵医行为、伤口愈合情况、二次手术率以及疼痛程度等方面的效果。结果远程护理干预后遵医行为、伤口愈合情况、行二次手术率方面观察组优于对照组(P<0.05),观察组疼痛管理方面干预后优于干预前(P<0.01)。结论远程护理干预能够提高手指屈肌腱断裂吻合术后患者的遵医行为,减少术后并发症,促进疾病早日康复。

关键词：远程护理干预遵医行为手指屈肌腱

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