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目的探讨促红细胞生成素（EPO）对肾性贫血大鼠肾脏的保护作用及其可能的作用机制。方法将实验大鼠随机分为对照组（NC组,n=18）和实验组（n=72）,采用腺嘌呤注射建立肾性贫血大鼠模型,再随机分为单纯贫血组（SA组）、铁剂＋促红素组（IR＋EPO组）、促红素组（EPO组）、铁剂组（IR组）。药物干预4周后,处死大鼠（心脏取血）,自动化血液分析仪检测血清肌酐（Scr）、尿素氮（Bun）、血红蛋白（Hb）、血细胞比容（Hct）;ELISA法检测铁调素（Hepcidin）。免疫组织化学染色法和Western blot法分别检测大鼠肾脏骨形态蛋白-6（BMP-6）、丝/苏氨酸激酶受体-1（SMAD-1）和SMAD-4的表达。结果 1一般指标的比较：与SA组相比较,IR＋EPO组和EPO组BUN、Scr显著降低（P〈0.01）;IR＋EPO组和EPO组Hb、Hct显著升高（P〈0.01）。2ELISA法检测示IR＋EPO组和EPO组铁调素显著降低（P〈0.01）。3病理学观察提示EPO可以减轻大鼠肾脏病理及功能改变。4免疫组织化学染色示各组大鼠肾小球细胞胞质和肾小管上皮细胞内均表达SMAD-4、SMAD-1、BMP-6。5Western blot进一步提示,与SA组相比,IR＋EPO组和EPO组SMAD-4蛋白表达量显著下调（P〈0.01）,IR＋EPO组和EPO组SMAD-1蛋白表达量下调（P〈0.05）,IR＋EPO组和EPO组BMP-6蛋白表达量显著上调（P〈0.01）。结论 EPO通过BMP/SMAD传导通路,抑制铁调素的表达及分泌,纠正贫血,发挥肾脏保护作用。

目的：观察促红细胞生成素（EPO）及/或进一步沉默 Omi/HtrA2表达时对缺氧复氧（H/R）心肌细胞的影响,探索相关抗细胞凋亡机制。方法培养乳鼠心肌细胞株（H9C2细胞）,分组（对照组、H/R 组及各浓度的 EPO 干预组）处理后,酶标仪检测各组细胞上清液中乳酸脱氢酶（LDH）释放率,Western blot 检测细胞内 cleaved caspase-3、Omi/HtrA2蛋白表达变化；并观察 Omi/HtrA2在胞质和线粒体的表达变化（转位情况）。再经脂质体法将 Omi/HtrA2特异性 siRNA 干扰片段转染至 H9C2细胞中,RT-PCR 和 Western blot 验证 siRNA 对 Omi/HtrA2表达的沉默效应后,分组同前干预,分别检测各组细胞 LDH 释放率及 cleaved caspase-3表达变化。结果与 H/R 组相比, EPO 干预组细胞上清液 LDH 释放减少,cleaved caspase-3表达减弱；H/R 组 Omi/HtrA2蛋白表达在胞质中表达较对照组增多（向胞质发生转位）,而 EPO（20 IU/mL）组其胞质转位减少。经 siRNA 干扰后,与 H/R 组相比,LDH 释放降低,cleaved caspase-3表达减弱,差异均有统计学意义（P 〈0.05）。结论EPO 可能通过减少 Omi/HtrA2蛋白的转位,抑制 caspases-3通路激活,而发挥细胞保护作用。

目的探讨缺氧诱导因子-1α（HIF-1α）和促红素（EPO）在糖尿病大鼠肾组织中的表达及其与糖尿病肾病的关系。方法用链脲佐菌素（STZ）制造糖尿病大鼠模型并在制模成功后4周和8周取肾组织，采用免疫组化方法及全自动图像分析系统检测糖尿病大鼠。肾组织中HIF-1α及EPO的表达。结果糖尿病大鼠肾小球及肾小管均有HIF-1α及EPO的表达，且随着造模时间的延长HIF-1α及EPO的表达逐渐增加。结论糖尿病肾病由于微循环障碍导致组织缺氧，从而使HIF-1α及EPO的表达上调。这也是糖尿病肾病出现微血管结构异常及新生血管形成从而导致糖尿病肾病发生、发展的可能原因。

目的探讨益肾保真方干预慢性肾衰竭营养不良的作用机制。方法采用二步5/6肾切除法复制大鼠慢性肾衰竭模型,随机分为正常组、模型组、尿毒清组、开同组及益肾保真方高、低剂量组。给药6周,观察血BUN、Scr、ALB、Hgb、EPO及Leptin水平;分析Leptin与EPO表达的相关性。结果模型组大鼠BUN、Scr及Leptin水平较正常组显著升高,ALB、Hgb及EPO水平显著降低。与模型组比较,益肾保真方组BUN、Scr及Leptin水平显著降低（P〈0.01）,ALB、Hgb及EPO水平显著升高（P〈0.01）;Leptin与EPO之间存在着显著的负相关（r=-0.681,P〈0.05和r=-0.676,P〈0.05）。结论益肾保真方干预CRF营养不良、提高血清白蛋白的机制可能与：降低氮质潴留,减轻毒素对蛋白合成的抑制有关;与改善肾功能,促进Leptin的排泄有关;与升高血清EPO水平,从而降低Leptin的分泌有关。

背景与目的促红细胞生成素（erythropoietin,EPO）对肿瘤细胞的具体作用存在争议。本研究旨在探讨细胞因子超家族成员EPO对肺腺癌A549细胞株生物学行为的影响。方法构建真核表达质粒pcDNA3.1（-）-hEPO,并转染肺腺癌A549细胞株。采用酶联免疫吸附（ELISA）法检测转染后目的基因的蛋白表达水平;MTT法和流式细胞仪检测转染后A549细胞生长、周期及凋亡率等生物学行为的变化;ELISA法检测转染后细胞VEGF表达水平的变化。结果成功构建真核表达质粒pcDNA3.1（-）-hEPO;转染后各检测时间点,EPO转染组细胞生长均明显受抑（P〈0.01）;流式细胞术分析表明,EPO转染组S期细胞比例明显高于对照组（P〈0.05）,且凋亡率也明显增高（P〈0.01）;EPO转染组VEGF表达量明显降低（P〈0.01）。结论EPO基因转染A549后有抑制细胞生长、促进凋亡的作用,并且还可抑制细胞表达VEGF。

目的观察葛根素对血管性痴呆（VD）大鼠海马中低氧诱导因子-1α和红细胞生成素表达的影响并探讨其可能机制。方珐采用大鼠双侧颈总动脉永久性阻断法（2-VO）建立VD的动物模型，SD大鼠随机分为假手术组、2-VO组和葛根素组，每组又分为1周、3周、6周、2月（n=6）四个时间点；应用Y型水迷宫实验测定动物的学习记忆能力，采用免疫组化法检测大鼠海马CA1区HIF～1α和EPO蛋白的表达。结果①2-VO组和葛根素组大鼠游全程时间和误入盲端次数均显著增加，但各时间点葛根素组大鼠的学习记忆成绩均显著优于2-VO组。②各时间点，2-VO组和葛根素组大鼠海马CA1区HIF-1α和EPO的表达均较假手术组明显增高，但葛根素组两种蛋白的表达均较2-VO组明显降低。结论葛根素可提高缺血脑组织细胞内氧浓度，改善学习记忆功能，对VD具有确切的保护作用。

目的 研究绞股蓝总皂甙(gypenoside,GP)对肾性贫血大鼠血浆促红细胞生成素(erythropoietin,EPO)含量的影响。方法 用腺嘌呤灌胃建立大鼠肾性贫血模型，治疗组加用GP。用胎鼠肝细胞法测定EPO。结果 治疗组肾功能明显改善，EPO含量明显升高。结论 GP具有改善肾功能，升高血浆EPO水平的作用，可应用于肾性贫血的治疗。

Erythropoietin （Epo） is a fundamental hormone in the regulation of hematopoiesis, and other secondary roles mediated by the binding of the hormone to its specific receptor （EpoR）, which leads to an activation of key signaling pathways that induce an increase in cell differentiation, apoptosis control and neuroprotection. It has been suggested that their ftmction depends on final conformation of glycosylations, related with affinity to the receptor and its half-life. The presence of EpoR has been reported in different tissues including central nervous system, where it has been demonstrated to exert a neuroprotective function against oxidative stress conditions, such as ischemic injury and neurodegenerative diseases. There is also evidence of an increase in EpoR expression in brain cell lysates of Alzheimer＇s patients with respect to healthy patients. These results are related with extensive in vitro experimental data of neuroprotection obtained from cell lines, primary cell cultures and hippocampal slices. Additionally, this data is correlated with in vivo experiments （water maze test） in mouse models of Alzheimer＇s disease where Epo treatment improved cognitive function. These stud- ies support the idea that receptor activation induces a neuroprotective effect in neurodegenerative disorders including dementias, and especially Alzheimer＇s disease. Taken together, available evidence suggests that Epo appears to be a central element for EpoR activation and neuroprotective properties in the central nervous system. In this review, we will describe the mechanisms associated with neuroprotection and its relation with the activation of EpoR in order with identify new targets to develop pharmacological strategies.

Although hypothermia therapy is effective to treat neonatal hypoxic-ischemic encephalopathy,many neonatal patients die or suffer from severe neurological dysfunction.Erythropoietin is considered one of the most promising neuroprotective agents.We hypothesized that erythropoietin combined with hypothermia will improve efficacy of neonatal hypoxic-ischemic encephalopathy treatment.In this study,41 neonates with moderate/severe hypoxic-ischemic encephalopathy were randomly divided into a control group（hypothermia alone for 72 hours,n = 20） and erythropoietin group（hypothermia ＋ erythropoietin 200 IU/kg for 10 days,n = 21）.Our results show that compared with the control group,serum tau protein levels were lower and neonatal behavioral neurological assessment scores higher in the erythropoietin group at 8 and 12 days.However,neurodevelopmental outcome was similar between the two groups at 9 months of age.These findings suggest that erythropoietin combined with hypothermia reduces serum tau protein levels and improves neonatal behavioral neurology outcome but does not affect long-term neurodevelopmental outcome.

Hypoxic-ischemic encephalopathy（HIE） is a disease that occurs when the brain is subjected to hypoxia,resulting in neuronal death and neurological deficits,with a poor prognosis.The mechanisms underlying hypoxic-ischemic brain injury include excitatory amino acid release,cellular proteolysis,reactive oxygen species generation,nitric oxide synthesis,and inflammation.The molecular and cellular changes in HIE include protein misfolding,aggregation,and destruction of organelles.The apoptotic pathways activated by ischemia and hypoxia include the mitochondrial pathway,the extrinsic Fas receptor pathway,and the endoplasmic reticulum stress-induced pathway.Numerous treatments for hypoxic-ischemic brain injury caused by HIE have been developed over the last half century.Hypothermia,xenon gas treatment,the use of melatonin and erythropoietin,and hypoxic-ischemic preconditioning have proven effective in HIE patients.Molecular chaperones are proteins ubiquitously present in both prokaryotes and eukaryotes.A large number of molecular chaperones are induced after brain ischemia and hypoxia,among which the heat shock proteins are the most important.Heat shock proteins not only maintain protein homeostasis; they also exert anti-apoptotic effects.Heat shock proteins maintain protein homeostasis by helping to transport proteins to their target destinations,assisting in the proper folding of newly synthesized polypeptides,regulating the degradation of misfolded proteins,inhibiting the aggregation of proteins,and by controlling the refolding of misfolded proteins.In addition,heat shock proteins exert anti-apoptotic effects by interacting with various signaling pathways to block the activation of downstream effectors in numerous apoptotic pathways,including the intrinsic pathway,the endoplasmic reticulum-stress mediated pathway and the extrinsic Fas receptor pathway.Molecular chaperones play a key role in neuroprotection in HIE.In this review,we provide an overview of the mechanisms of HIE and discuss the various treatment strategies.Given their critical role in the disease,molecular chaperones are promising therapeutic targets for HIE.