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1.
Objective: To detect the expressions of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in purified rat choroid plexus epithelial cells in vitro. Methods: Primary and passage choroid plexus epithelial cells were obtained from newborn, one-day Spragne-Dawley rats. The expressions of BDNF and NGF were measured by qRT-PCR and Western blottingting. The secretions of BDNF and NGF were detected by ELISA. Cell supematants of primary cells, purified cells and passage 1 cells were harvested. Results: The expression of BDNF in the purified cells was significantly lower than that in the primary cells (P〈0.05), and it in the primary cells and the purified cells was significantly higher than that in the passage 1 cells (P〈0.05). The expression of NGF was significantly higher in the purified cells than in the primary cells and the passage 1 cells (P〈0.05). It in the passage 1 cells was significantly higher than that in the primary cells (P〈0.05). Conclusion: The time of CPECs transplantation for central nervous system diseases should be selected based on their secretory function and features,which could lead to better and more effective treatment.  相似文献   

2.
In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.  相似文献   

3.
Expression of heregulin and ErbB receptors in mesenchymal   总被引:1,自引:0,他引:1  
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4.
To examine the protective effect of insulin on reoxygenation-induced injury and explore the underlying mechanisms, the model of anoxia/reoxygenation (A/R) injury was established by inducing anoxia for 2 h and reoxygenation for 4 h in cultured cardiomyocytes of neonatal rats. The rats were randomized to four groups receiving vehicle, insulin, LY294002, insulin plus LY294002 at the onset of reoxygenation after 2 h of anoxia. At the end of reoxygenation of 4 h, activity of lactate dehydrogenase (LDH) and content of malondialdehyde (MDA) were spectrophotometrically determined, apoptosis of cardiomyocytes were detected by using TUNEL and DNA Ladder, and Western blotting was employed to examine the expression of phosphorylated Akt in all groups. Our results showed that compared with vehicle-treated group, activities of LDH, contents of MDA, apoptosis index (AI) were significantly decreased, and expression of phosphorylated Akt was increased significantly in insulin-treated group. However, changes in LDH, MDA, AI and phosphorylated Akt resulting from insulin were attenuated or abolished by LY294002 (PI3K inhibitor). These data strongly suggest that early administration of insulin at reoxygenation protects cardiomyocytes from reoxygenation-induced apoptosis through PI3K/Akt signaling pathway.  相似文献   

5.
Objective To investigate the effect of n-butanol extract from Potentilla anserina (NP) intervention on hypoxia-induced Ca2+ overload and SERCA2 expression of rat cardiomyocytes. Methods Primary cultured myocardial cell from SD neonatal rat (1-3 d) was used in the establishment of hypoxia model. After hypoxia for 3 h, the Ca2+ concentration of myocardial cells was measured with fura-2/AM fluorescent probe, and the biochemical indicator intracellular Ca2+-ATPase was examined and the mRNA and its protective protein levels of the sarcoplasmic reticulum (SR) Ca2+-ATPases (SERCA2) were assayed with RT-PCR, Western-blotting, and immune-cytochemical staining in each group. Results The results showed that NP decreased Ca2+ concentration, increased the activity of Ca2+-ATPase, and improved the mRNA and protein expression of SERCA2 in hypoxia-injured myocardial cells as compared with the model group. Conclusion These results indicate that NP could attenuate the Ca2+ overload. The mechanism might be explained as that NP could elevate the SERCA2 level, increase the activity of myocardium in rats, and further enhance the capacity of SR Ca2+ re-uptake.  相似文献   

6.
Objective To develop a cellular model of preconditioning by a brief period of hypoxia in isolated guinea pig cardiomyocytes and to determine whether or not an ATP sensiti ve K(+) (K(ATP)) channel is involved in ischemic precond itioning. Methods Single myocytes were isolated from the ventricle of adult guinea pigs.The expe rimental chamber allowed the cells to be exposed to low O(2)pressure.During h ypoxic preconditioning, the cells were equilibrated with normaxic solution for 1 0 minutes and then exposed to hypoxia for 5 minutes, followed by 10 minutes of re oxygenation.The cells were then subjected to 20-180 minutes of hypoxia and reoxygenation.Ionic currents were studied with the patch clamp technique in w hole-cell and cell-attached configurations. Results A 5-minute hypoxic preconditioning offered a significant protection from cell i n jury in subsequent hypoxia-reoxygenation.After a latency of more than 15 minu tes, hypoxia induced a time-independent outward K(+) current which could be blo cked by 5 μmol/L glibenclamide.At 10 mV, the current increased from 78 ±1 5 pA to 1581±153 pA (P<0.01, n=18).However, the latency to develop K(ATP) channel currents (I(KATP)) was greatly shortened in preconditioned c ells, and the current was increased acceleratively.At 10 mV, the current more than 4 nA was recorded in preconditioning cells.In the single channel record ings, the time interval from the first channel opening to maximum opening was also markedly abbreviated in preconditioned cells.Conclusion Isolated guinea pig cardiomyocytes can be preconditioned with a brief period of hypoxia.This hypoxic preconditioning may modify the K(ATP) channel, and make the channel open more readily during the second hypoxia.  相似文献   

7.
Objective:Carbamylated EPO(CEPO)is a derivative of erythropoietin(EPO)by subjecting it to carbamylation.It does not stimulate erythropoiesis,but effectively protects tissue from injury.The present study was to investigate the effect of CEPO treatment using in vitro models of hypoxia/reoxygenation(H/R).Methods:Cardiomyocytes were exposed to hypoxia(95% N2 and 5% CO2)for 1 hour followed by 4 hours of reoxygenation(95% O2 and 5% CO2).CEPO was administered after hypoxia,just before reoxygenation.The apoptotic cardiomyocytes were determined by flow cytometry.The level of protein was assessed by western blot analysis.Results:CEPO treatment significantly decreased the apoptotic cardiomyocytes by 54.20% compared with H/R group.Western blot analysis showed that CEPO administration increased the level of Bcl-2(an antiapoptotic protein)by 62.22% compared with H/R group.Conclusion:Acute administration of CEPO protected cardiomyocytes from H/R-induced apoptosis.CEPO protected cardiomyocytes with a concomitant upregulation of Bcl-2 after H/R injury.  相似文献   

8.
Summary: To study the angiogenic potency of hypoxia-prestimulated bone marrow stromal cells(BMSCs) when transplanted into acute myocardial infarction models of rats. BMSCs were cultured under hypoxia condition for 24 h. Their expression of VEGF was investigated. The rat acute myocardial infarction models were made by coronary artery ligation and divided into 3 groups at random.In normoxia group, twice-passaged BMSCs were labeled with Bromodeoxyuridine (BrdU) and then implanted into the infarction regions and ischemic border of the recipients in 4 weeks. The rats in hypoxia group were implanted with hypoxia-prestimulated BMSCs. In control group, the model rats received only DMEM medium injection. Six-weeks after AMI, the infarction regions were examined to identify the angiogenesis and the expression of the VEGF. Our results showed that viable cells labeled with BrdU could be identified in the host hearts. The infarction regions in normoxia and hypoxia groups had a greater capillary density and increased VEGF expression than the regions in control group. The capillary density and VEGF expression in hypoxia group were higher than in normoxia group. It is concluded that the enhanced expression of VEGF in BMSCs could be induced by ex vivo hypoxia stimulation. BMSCs implantation promoted the angiogenesis in myocardial infarction tissue via supplying exogenic VEGF. Angiogenic potency of bone marrow stromal cells was improved by ex vivo hypoxia prestimulation though the enhanced VEGF expression.  相似文献   

9.
Arsenic trioxide (ATO) can induce cellular apoptosis ,and inhibit the activities of multiple myeloma (MM)cells in vitro, but how it works is not very clear. Recent studies showed that ATO worked on the voltagedependent potassium channel and L-type calcium channel in myocardial cells, but the effect of ATO on ion channels of tumor cells was rarely reported. As the potassium channel plays an important role in controlling cell proliferation, we studied the effects of ATO on the voltage-dependent potassium current (Ikv) of the voltage-dependent potassium channel in an MM cell line, and probed into the relationship between changes of the Ikv caused by ATO and cell proliferation.  相似文献   

10.
Effects of glycine and methylprednisolone on hemorrhagic shock in rats   总被引:5,自引:0,他引:5  
Background Methylprednisolone (MP), a synthetic glucocorticosteroid, has been broadly studied in experiments on endotoxin-induced shock and septic shock. This study was designed to ascertain whether glycine and MP can protect against organ injury and death caused by hemorrhagic shock, and to elucidate the underlying mechanisms of these protective effects in rats.Method To establish a shock model, Wistar rats were bled to maintain mean arterial pressure at 30-50 mmHg for 1 hour and subsequently resuscitated with the shed blood and normal saline. Just prior to resuscitation, the rats were randomly assigned to four groups: sham group (operation performed without inducing shock), shock group, shock+glycine group (glycine injected at the beginning of resuscitation) and shock+MP group (MP injected at the beginning of resuscitation).Results ① Seventy-two hours after resuscitation, the survival rate of rats from the shock group had decreased to 20%, while the survival rates of rats from the shock+glycine and shock+MP groups were 77.8% and 80%, respectively. The difference was significant (P<0.05). ② Eighteen hours after resuscitation, pathological alterations in the organs of the rats were apparent. In rats from the shock group, edema, interstitial leukocyte infiltration, and cellular degeneration occurred in the liver, lungs, kidneys, and heart. Glycine and MP reduced these pathological changes significantly. ③ Eighteen hours after resuscitation, the levels of creatine phosphokinase, transaminases, and creatine were elevated significantly in rats from the shock group, indicating injury to the heart, liver, and kidneys, while these levels were elevated only slightly in the shock+glycine and shock+MP groups. The differences were significant (P<0.01). ④ There were significant increases in intracellular calcium and production of tumor necrosis factor (TNF-α) by isolated Kupffer cells stimulated by endotoxin after hemorrhagic shock. These changes were completely prevented by glycine and MP (P<0.01). Conclusion Glycine and MP reduce organ injury and mortality caused by hemorrhagic shock by preventing increase of intracellular calcium levels in Kupffer cell, suppressing Kupffer cell activation, decreasing the production of TNF-α by Kupffer cells, and blocking systemic inflammatory responses.  相似文献   

11.
甘氨酸对SD乳鼠心肌细胞缺氧损伤的保护作用   总被引:6,自引:1,他引:5  
目的探讨甘氨酸对缺氧心肌细胞的保护作用.方法台盼蓝排斥实验检测细胞的存活率;生化分析仪检测培养液中心肌细胞乳酸脱氢酶(LDH)的释放量;激光共聚焦显微镜技术检测缺氧后心肌细胞内游离钙的变化.结果甘氨酸可以明显提高缺氧后心肌细胞的存活率;减少缺氧后心肌细胞LDH的释放且作用随其浓度的升高而增强;减轻缺氧后心肌细胞的钙超载.结论甘氨酸提高缺氧后心肌细胞的存活率,减少LDH释放,减轻钙超载,对心肌细胞有保护作用.  相似文献   

12.
目的研究色满卡林(Cromakalim,CRK)对缺氧复氧致大鼠乳鼠心肌细胞损伤的保护作用,并探讨其机制。方法用原代培养的Sprague—Dawley(SD)大鼠乳鼠心肌细胞建立缺氧2h复氧30min的损伤模型。采用乳酸脱氢酶(LDH)试剂盒测培养液中LDH的活性;采用黄嘌呤氧化酶法测定细胞内超氧化物岐化酶(SOD)活性;硫代巴比妥酸显色法测定细胞内丙二醛(MDA)含量;AV—PI双标记后应用流式细胞仪检测细胞的凋亡率。结果色满卡林对缺氧复氧造成的心肌细胞损伤有保护作用,表现为可以对抗缺氧复氧引起的LDH活性增加、MDA含量增加、SOD活性下降、凋亡率增加。结论色满卡林对缺氧复氧致培养大鼠乳鼠心肌细胞的损伤具有保护作用,此作用与抑制脂质过氧化、减少心肌细胞凋亡有关。  相似文献   

13.
[目的] 探讨栀子苷预处理对H9C2心肌细胞缺氧/复氧损伤的影响及机制。[方法] 体外培养H9C2心肌细胞,制备缺氧/复氧损伤模型。实验分为正常对照组,缺氧/复氧模型组,栀子苷预处理组。分光光度法测定细胞培养液中肌酸激酶(CK)、乳酸脱氢酶(LDH)、丙二醛(MDA)含量以及过氧化物歧化酶(SOD)活性,四甲基偶氮唑蓝(MTT)法检测细胞存活率,Annexin V-FITC/PI双染法流式细胞术测定细胞凋亡率。[结果] 与模型组比较,栀子苷预处理组能明显减少心肌细胞CK、LDH的漏出量,提高SOD活力,降低MDA含量,同时提高心肌细胞的存活率,减少心肌细胞的凋亡。[结论] 栀子苷预处理对H9C2心肌细胞的缺氧/复氧损伤具有保护作用,其机制可能与增强心肌抗氧化能力、清除氧自由基以及抑制心肌细胞凋亡有关。  相似文献   

14.
目的 观察UcnⅠ对成年大鼠缺氧/复氧损伤心肌细胞钙离子的影响.方法 通过Langendorff离体心脏灌注系统,用Ⅱ型胶原酶逆行灌注法分离成年大鼠心肌细胞,培养20 h后随机分为正常组(N组)、缺氧/复氧组(L/R组)、UrocortinⅠ组(UcnⅠ组)、5-羟葵酸+UrocortinⅠ组(5- HD+UcnⅠ组).各处理组心肌细胞加入Fluo - 3/AM荧光探针,用激光共聚焦显微镜检测细胞内钙的荧光强度.结果 I/R组心肌细胞内钙离子浓度较N组高(P<0.05),UcnⅠ组较N组荧光强度明显增强(P<0.01),而5- HD+UcnⅠ组心肌细胞内钙离子荧光强度与UcnⅠ组比较明显降低(P<0.05).结论UcnⅠ可使成年大鼠缺氧/复氧损伤心肌细胞内钙离子浓度升高,5- HD则可阻断UcnⅠ的作用,提示UcnⅠ导致缺氧/复氧后心肌细胞钙离子浓度的升高可能跟ATP敏感性钾通道开放有关.  相似文献   

15.
目的 观察舒芬太尼预处理对H9C2细胞缺氧复氧损伤后细胞活力和乳酸脱氢酶(LDH)的影响及其浓度依赖性。方法 采用培养的H9C2心肌细胞进行实验,以细胞处于缺氧环境而后进行复氧作为损伤模型。细胞分为正常对照组(NC组)、缺氧复氧损伤对照组(HR组)、舒芬太尼预处理组(SF组)。根据不同浓度舒芬太尼(1×10-11、10-10、10-9、10-8、10-7和10-6mol/L),SF组又分为SF11、SF10、SF9、SF8、SF7、SF6组,每组6孔。处理后MTT法测定细胞活力,检测培养液上清中乳酸脱氢酶(LDH)活力。结果 培养的H9C2细胞经过缺氧3 h复氧3 h之后出现明显的损伤。与NC组相比,HR组培养液上清中LDH活力明显升高、细胞活力显著下降。给予不同浓度的舒芬太尼预处理15 min后再进行缺氧复氧,这种损伤可被抑制。与HR组相比,舒芬太尼预处理组培养液上清中LDH活力降低、细胞活力提高,并发现当舒芬太尼的浓度达到10-9mol/L时其保护效果已基本达到最大,浓度再增大时,保护效果的增加已无显著性差异。结论 舒芬太尼预处理可明显增强H9C2细胞抗缺氧复氧损伤能力,具有浓度依赖性。  相似文献   

16.
目的:研究神经再生素(NRF)对纯化培养心肌细胞缺氧/复氧损伤的保护作用及机制。方法:采用纯化培养的心肌细胞建立缺氧/复氧损伤模型,观察心肌细胞形态学变化,测定细胞超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)和线粒体脱氢酶含量改变,探讨NRF对心肌细胞缺氧/复氧损伤的保护作用。结果:缺氧/复氧损伤后,胞体折光性下降,突起缩短或消失,搏动减弱或消失,NRF各剂量组心肌细胞形态均较缺氧/复氧组明显改善,NRF各剂量组SOD、MDA、线粒体脱氢酶活性与缺氧/复氧组比较差异有统计学意义(P<0.01)。结论:神经再生素具有明显的抗缺氧/复氧损伤,保护心肌作用,其机制可能与其抑制心肌脂质过氧化损伤有关。  相似文献   

17.
韩坤  王丹萍  袁磊 《重庆医学》2015,(31):4333-4335
目的:探究胡芦巴碱(T RG )对缺氧/复氧乳鼠心肌细胞的保护作用及其机制。方法原代培养SD乳鼠心肌细胞,随机分成3组:正常对照(Control组)、缺氧/复氧组(H/R组)和TRG加缺氧/复氧组(TRG+ H/R组);采用流式细胞术分别检测TRG对缺氧/复氧乳鼠心肌细胞凋亡和线粒体膜电位的影响;采用超氧化物歧化酶(SOD)和丙二醛(MDA)试剂盒检测SOD活性和MDA水平,蛋白免疫印迹法(Western blot)检测procaspase‐9、cleaved caspase‐9、procaspase‐3和cleaved caspase‐3蛋白水平。结果 TRG能够显著降低缺氧/复氧乳鼠心肌细胞凋亡率(P<0.05),增强SOD活性(P<0.05),减少MDA的生成(P<0.05),稳定线粒体膜电位( P<0.05),促进caspase‐9和caspase‐3的活化。结论 T RG可减轻缺氧/复氧对乳鼠心肌细胞的损伤,其机制可能与抗脂质过氧化和稳定线粒体膜电位有关。  相似文献   

18.
目的研究卡维地洛对缺氧/复氧损伤心肌细胞的保护作用,并探讨其可能的作用机制。方法新生1-3 d的Sprague-Dawley鼠,原代分离,培养其心肌细胞72 h后,随机分为正常对照组、单纯缺氧/复氧组及卡维地洛 缺氧/复氧组。先将培养板中的心肌细胞缺氧(氧浓度<1%)120 min,再复氧30 min,造成缺氧/复氧损伤模型,测定细胞存活率;抽取细胞培养上清液测定乳酸脱氢酶(LDH)、磷酸肌酸激酶同工酶(CK-MB);并破碎细胞,测定丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果卡维地洛 缺氧/复氧组的细胞培养液中LDH和CK-MB漏出量分别为(32.32±1.46)和(28.33±2.12)U/L,均显著低于缺氧/复氧组[(50.28±1.22)和(42.45±3.22)U/L,P值均<0.05];卡维地洛 缺氧/复氧组的细胞存活率为(70.21±2.12)%,显著高于缺氧/复氧组[(58.39±3.22)%,P<0.05]。卡维地洛 缺氧/复氧组的细胞内MDA含量为(5.32±0.32)nmol/mL,显著低于缺氧/复氧组[(8.32±0.42)nmol/mL,P<0.05];SOD活性为(10.32±0.42)U/mL,显著高于缺氧/复氧组[(7.42±0.20)U/mL,P<0.05]。结论卡维地洛对心肌细胞缺氧/复氧损伤具有保护作用,能清除氧自由基,提高心肌细胞抗氧化能力。  相似文献   

19.
刘丹  尹东  汤蕾  孙惦  许旻  何明 《第三军医大学学报》2012,34(17):1707-1710
目的探讨14-3-3γ基因在LPS预处理对抗心肌细胞缺氧/复氧(A/R)损伤中的作用。方法构建pSU-PER/14-3-3γRNA干扰重组质粒,转染入心肌细胞,分为5组:对照组、A/R组、LPS+A/R组、pSUPER+LPS+A/R组、pSUPER/14-3-3γ+LPS+A/R组。Western blot检测14-3-3γ蛋白表达,生化自动分析仪测定乳酸脱氢酶(LDH)活性,MTT法测定细胞存活率,流式细胞仪检测细胞凋亡,线粒体肿胀实验检测线粒体通透性转换孔(mPTP)开放。结果 A/R损伤使细胞存活率下降,LDH升高,细胞凋亡增加,mPTP开放;LPS预处理可使14-3-3γ表达明显增加,通过抑制mPTP开放,对A/R损伤的细胞有保护作用;pSUPER/14-3-3γRNA干扰重组质粒通过抑制14-3-3γ蛋白表达,取消LPS预处理的保护作用。结论 LPS预处理可对抗心肌细胞缺氧/复氧损伤,其机制与上调14-3-3γ,从而抑制mPTP开放有关。  相似文献   

20.
目的 研究硫酸镁对纯化培养乳鼠心肌细胞缺氧/复氧损伤的保护作用及其作用机制。方法 采用培养乳鼠心肌细胞建立缺氧/复氧损伤模型,实验分为五组:正常对照组、缺氧/复氧损伤模型组、缺氧/复氧损伤+MgSO4(2.2、4.0、7.2mmol/L)组。分别用黄嘌呤氧化酶法测定细胞内SOD活性,硫代巴比妥酸法测定细胞内MDA含量,MTT染色法测定心肌细胞活力并测定培养液中LDH含量的变化。结果 硫酸镁能显著提高细胞内SOD的活性,降低MDA、LDH的含量并可提高心肌细胞的活力。结论 硫酸镁具有明显的抗缺氧/复氧损伤、保护心肌细胞的作用。  相似文献   

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