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目的初步观察经体外循环心脏术后多脏器功能障碍综合征(MODS)伴急性肾功能衰竭(ARF)患者的氧化应激水平,为临床治疗提供理论基础。方法测定16例经体外循环心脏术后MODS伴ARF患者及16例健康人的血清丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、总抗氧化能力(TAC),同时对患者进行MODS评分,并将评分与氧化应激参数进行相关性分析。结果116例患者,8例存活,8例死亡(病死率50%);2与健康对照组相比,MODS伴ARF组在性别、年龄方面无显著性差异,TAC,SOD代偿性升高,但GSH-Px明显下降,MDA显著升高。3MDA同MODS评分呈正相关;GSH-Px同MODS评分呈负相关。SOD、TAC同评分无明显相关性。结论1经体外循环心脏手术后MODS伴ARF的患者发生了氧化应激。2监测MDA和GSH-Px有助于判断病情。3在MODS伴ARF的治疗中,有必要采用各种治疗措施恢复机体的氧化抗氧化。 相似文献
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血管内皮生长因子对肾小管上皮-间充质细胞转化的作用及其与骨形成蛋白-7、分化抑制因子表达的关系 总被引:13,自引:0,他引:13
目的探讨血管内皮生长因子(VEGF)对肾小管上皮-间充质细胞转化(EMT)的作用及其与骨形成蛋白-7(BMP-7)、分化抑制因子(Id)2、Id3表达的关系。方法体外培养的人肾小管上皮细胞(HK-2)经转化生长因子-β1(TGF-β1,5ng/ml)与不同浓度VEGF165(0.1、1、10、100ng/ml)共同作用,或TGF-β1(5ng/ml)与血管内皮生长因子受体-1(VEGFR1)抗体(10μg/ml)共同作用48h后,免疫组织化学双染方法检测细胞α-平滑肌肌动蛋白(α-SMA)、E-钙黏素表达,实时荧光定量PCR法、Westernblot法检测细胞α-SMA、BMP-7、Id2和Id3的表达。TGF-β1(5ng/ml)、VEGF165(100ng/ml)与激活素受体样激酶-6/Fc嵌合体(Alk6/FcChimera)(2μg/ml,中和内源性BMP-7)共同作用48h后,Westernblot法检测细胞α-SMA、Id2的表达情况。结果TGF-β1作用后,α-SMA表达比正常对照显著增强(P<0.05),E-钙黏素、BMP-7、Id2及Id3的mRNA及蛋白质表达均显著减弱(P<0.05)。VEGF165以浓度依赖方式增强BMP-7及Id2蛋白表达,而显著降低TGF-β1上调α-SMA表达的作用(P<0.05)。加入VEGFR1抗体(10μg/ml)后,TGF-β1上调α-SMA表达的作用显著增强(P<0.05),而E-钙黏素、BMP-7、Id2表达显著减弱(P<0.05)。TGF-β1 VEGF165 Alk6/FcChimera共同作用后α-SMA蛋白表达比TGF-β1 VEGF165共同作用后显著增强(P<0.05),而Id2表达差异无显著性。结论VEGF165可抑制TGF-β1诱导HK-2细胞发生EMT;其机制可能与BMP-7和Id2表达上调有关,而与Id3表达变化无关。Id2表达增强可能与VEGF165的直接作用有关,而与BMP-7无关。 相似文献
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四种气管上皮细胞分离培养方法的比较研究 总被引:2,自引:0,他引:2
目的:比较四种不同的方法在培养气管上皮细胞中的异同,改进其培养技术,为组织工程气管提供种子细胞。方法:用两步酶消化法(使用0.1% Dispase 4℃消化18h后,用0.25%的胰酶37℃消化5min)、Dispase冷消化法(用0.1%Dispase 4℃消化18h)、胰酶温消化法(0.25%的胰酶37℃消化10min)和机械刮刷法四种方法分离、培养兔气管上皮细胞,测定分离细胞的数量和纯度。结果:两步酶消化法、Dispase冷消化法较其他两种方法得到的气管上皮细胞纯度高,细胞状态好;Dispase冷消化法得到细胞数量较其他方法少,其余三种方法得到的细胞数统计学上不存在差异。结论:两步酶消化法较其他方法所得细胞数量多、纯度高、细胞成活率高,是一种较好的气管上皮细胞体外分离培养方法。 相似文献
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Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway. 相似文献
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目的 前瞻性观察连续性血液净化(CBP)对心脏术后多脏器功能障碍综合征(MODS)存活者与死亡者炎性介质和氧化应激指标的影响.方法 16例心脏术后MODS伴ARF的患者使用HF700型聚砜膜血液滤过器行CBP治疗,8例存活(A组),8例死亡(B组);分别在治疗前(0h)和治疗后2、6、12、24和48h取血检测两组患者血清TNF-α、IL-6、IL-8、IL-4、丙二醛(MDA)、超氧化物歧化酶(SOD)和总抗氧化能力(TAC)等指标的变化.结果 CBP治疗2h后A组促炎因子TNF-α、IL-6迅速下降,24h后IL-8明显下降,而死亡组治疗过程中上述炎性介质水平较治疗前无明显变化;两组抗炎因子IL-4在CBP治疗过程中较治疗前有所下降,但无明显统计意义.A组TAC在CBP治疗6h后明显下降,MDA在12h后明显下降,SOD在24h后明显下降;B组SOD、TAC在治疗2h后即开始明显下降,MDA在48h的治疗过程中持续保持高水平,较治疗前无明显下降.结论 CBP有助于改善MODS患者促炎因子与抗炎因子的平衡,减轻炎性损伤.CBP能改善MODS患者的氧化应激,减轻氧化损伤.在CBP治疗过程中,TNF-α、IL-6、IL-8、MDA浓度持续高水平及SOD早期下降者预后差;动态监测上述指标可能有助于判断心脏术后MODS患者的预后. 相似文献
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目的观察水盐限制联合利尿治疗对CAPD患者容量超负荷的疗效。方法第四军医大学西京医院血液净化中心CAPD52例符合条件的患者随机分为A、B两组,A组单纯水盐限制,B组在水盐限制的基础上,加服速尿120~240mg/日,分2次口服,检测治疗前及治疗1月后体重、平均动脉压、尿量、超滤量、浮肿程度、心胸比例等变化。结果①较治疗前相比,A组的体重、平均动脉压、心胸比例均有所前下降,但无统计学意义,平均尿量和平均超滤量无变化。B组的体重、平均动脉压、平均尿量、心胸比例均较治疗前明显下降(P<0.05),其中体重和平均尿量在两组间差异具有显著性(P<0.05);②两组的水肿程度均有不同程度的下降,B组更为明显。③A组总有效率为53.8%,B组总有效率为84.7%。两组相比总有效率差异有统计学意义(P<0.05)。结论单纯限制水盐摄入或联用利尿治疗均能改善CAPD患者容量超负荷状况,但后者的效果更明显,水盐限制基础上加用利尿是治疗CAPD患者容量超负荷的安全有效的方法。 相似文献
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Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway. 相似文献
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