星形细胞瘤中Ki-67,VEGF,bcl-2,cyclin-D1及p16的免疫组化检测

目的 观察正常大脑组织和星形细胞瘤组织（I－Ⅳ）中Ki-67、VEGF、bcl-2,cyclin-D1与p16的表达，探讨其辅助诊断的意义。方法 应用免疫组化检测13例正常脑组织和58例星形细胞瘤组织中Ki-67,VEGF,bcl-2,cyclin-D1和p16的表达。结果经χ^2检验和单因素方差分析。结果 Ki-67和VEGF在正常大脑组织中均不表达，而在所有级别的星形细胞瘤中均表达，差异极显著（P＜0．01。随着星形细胞瘤恶性程度的增高，Ki-67的表达增强，VEGF表达阳性的病例增加；肿瘤组织中微血管的形态亦出现相应的变化，每两组间的差异极显著（P＜0．01）。bcl-2在4个实验组中均表达，各组间表达差异显著（P＜0．01），且随着肿瘤恶性程度的增高表达增强。cyclin-D1的表达阳性率各组间差异不显著（P＞0．05）。正常脑组织中p16有一定的表达，阳性率69．2％；在转化为肿瘤细胞后p16的阳性率反而升高。肿瘤组织中，总的趋势是随着肿瘤恶性程度的增高p16的表达降低。结论 临床病理诊断过程中，Ki-67,bcl-2的免疫组化检测可对星形细胞瘤的分级诊断提供非常有意义的依据。而VEGF的作用需结合微血管形态的变化一起考虑。cyclin-D1和p16的免疫组化检测不够敏感，故辅助诊断意义不大。     

人脑星形细胞肿瘤bcl-2基因表达与预后的关系

目的:探讨星形细胞肿瘤组织中bcl-2基因表达情况及其与肿瘤恶性程度和患者预后的关系。方法:采用免疫组织化学法检测60例星形细胞肿瘤组织中bcl-2基因表达情况.并分析其与肿瘤恶性程度和患者预后的关系。结果:60例肿瘤组织中bcl-2基因表达阳性率为50％,不同级别的肿瘤之间差异不显著(P>0.05),但其表达强度在不同级别肿瘤之间却有显著差异(P<0.05),高度恶性肿瘤bcl-2基因表达较强;预后分析显示bcl-2基因表达强度较高组的生存率较低(P<0.01),结论:星形细胞肿瘤组织中bcl-2基因表达上调在肿瘤发生、发展乃至间变的过程中可能起重要的作用.bcl-2基因表达强度可作为反映星形细胞肿瘤患者预后的重要指标之一。     

脑出血周围组织细胞凋亡与bcl-2及bax蛋白表达的关系

目的：探讨脑出血灶周围组织中bcl-2，bax蛋白表达和细胞凋亡的关系。方法：SD大鼠70只。随机分为两组（实验组和对照组）。实验组采用胶原酶诱导大脑尾状核脑出血模型，分别于术后第6h、12h、24h、48h、72h、7d、14d，7个时相点（每个时相点5只）处死大鼠，运用TUNEL法、免疫组化SP技术，检测血肿周围脑组织中细胞凋亡及bcl-2．bax蛋白表达。结果：实验组细胞凋亡、bcl-2，bax蛋白表达与对照组有非常显著性差异（P〈0．01）．高峰期分别为脑出血术后第6h、48h。bcl-2蛋白表达与凋亡阳性细胞数呈负相关（r=-0．7628，P〈0．05），bax蛋白表达与凋亡阳性细胞呈正相关（r=0.8438，P〈0．01）。结论：脑出血灶周围脑组织中存在细胞凋亡，bcl-2，bax蛋白对凋亡具有调控作用。     

白藜芦醇诱导KG-1细胞凋亡作用与bcl-2／bax表达相关性研究

本研究观察白藜芦醇（RES）体外诱导KG-1细胞凋亡的作用，探讨白藜芦醇诱导白血病细胞凋亡的可能作用机制。以不同浓度的白藜芦醇作用于KG-1细胞，用噻唑蓝（MTT）比色法分析细胞生长状态；透射电镜观察KG-1细胞凋亡的形态学变化；流式细胞术（FCM）测定细胞凋亡与周期分布；半定量RT-PCR、流式细胞技术检测细胞bel-2、bax表达水平。结果表明：白藜芦醇可明显抑制KG-1细胞增殖（P〈0．05），与对照组比较，白藜芦醇作用后KG-1细胞发生S期阻滞（P〈0．01），细胞凋亡增高（P〈0．01），bcl-2表达下调（P〈0．05），而bax表达明显上调（p〈0．01）。结论：白藜芦醇可诱导KG-1细胞凋亡，其机制可能与下调bcl-2、上调bax表达水平有关。     

细胞凋亡与bcl—2在皮肤鳞形细胞癌中的表达及意义

目的：研究人类皮肤肿瘤中细胞凋亡相关基因bcl-2的表达,探讨癌组织中凋亡和bcl-2的关系。方法：应用三羟基末端标记法和免疫组化（SABC）法原位观察了40例皮肤癌中细胞凋亡与bcl-2蛋白的表达,以10例正常组织作对照。结果：细胞凋亡广泛存在于皮肤鳞吕中和正常组织中,皮肤鳞癌中细胞凋亡明显高于正常组织（P＜0．05）;皮肤鳞癌中细胞凋亡与bcl-2阳性表达有显著差异（P＜0．01）。结论：皮肤癌组织中bcl-2与细胞凋亡关系密切,bcl-2有抑制细胞凋亡的作用。,     

人脑星形细胞瘤中EphA2表达与肿瘤血管生成关系的研究

目的探讨酪氨酸蛋白激酶受体EphA2在人脑星形细胞瘤中的表达及其与肿瘤血管生成的关系。方法用免疫组化方法测定78例人脑星形细胞瘤和8例正常脑组织（NB）中EphA2蛋白表达情况。用免疫组化方法检测肿瘤微血管密度（MVD）。结果EphA2蛋白阳性染色主要定位于肿瘤细胞胞浆和细胞膜,呈棕黄色颗粒,肿瘤血管内皮细胞也呈阳性表达。在78例星形细胞瘤中,EphA2阳性表达率为93．6％,而正常脑组织中无EphA2表达,二者差异有统计学意义（P〈0．01）。而且随着肿瘤恶性程度增加,EphA2蛋白染色强度和阳性细胞数均明显升高,高级别星形细胞瘤（Ⅲ～Ⅳ）与低级别星形细胞瘤（Ⅰ～Ⅱ）相比差异有统计学意义（P〈0．05）。随着EphA2阳性表达强度增加,肿瘤组织的MVD也逐渐增加,从0～3级分别为（19．65±8．12）个／mm^3、（27．50±11．36）个／mm^3、（40．28±12．51）个／mm^3和（61．44±13．80）个／mm^3,组间差异有统计学意义（F=6．308,P=0．001）。EphA2表达与MVD显著相关（r=7．094,P〈0.01）。结论EphA2可作为判定人脑星形细胞瘤恶性程度的重要指标,与肿瘤微血管生成相关,有可能成为星形细胞瘤治疗的一个新靶点。     

甲状腺乳头状癌中Livin mRNA与bcl-2的表达及相关性研究

目的研究凋亡抑制基因Livin和bcl-2在甲状腺乳头状癌（PTC）组织中的表达对肿瘤细胞凋亡的影响及两者的相关性，探讨Livin在pTC发生、发展和细胞凋亡调控中的作用。方法分别采用逆转录聚合酶链反应（RT-PCR）和免疫组织化学法检测32例PTC组织中Livin mRNA和bcl-2蛋白的表达。结果Livin mRNA和bcl-2蛋白在PTC组织中的阳性表达率分别为62．50％（20／32）和53．12％（17／32）。Livin和bcl-2的高表达与PTC的淋巴转移密切相关（P〈O．05），而与患者性别、年龄、包膜是否完整和临床分期等均无相关性（P均〉O．05）。相关性检验表明Livin与bcl-2表达无相关性（r=0．178，P〉0．05）。结论Livin在PTC组织中的高表达提示其可能参与PTC的发生和发展，可作为判断其预后的重要参考指标。Livin可能与bcl-2在PTC细胞凋亡的调控方面不起着协同作用。     

肺癌组织芯片中Stat3、bcl-2和VEGF表达与临床病理的关系

目的：通过检测肺癌组织芯片中Stat3、bcl-2和VEGF的表达，探讨它们在肺癌的发生发展及浸润转移中的作用，为肺癌的早期诊断、预后判断提供一定的理论依据。方法：应用组织芯片技术及免疫组织化学方法检测正常肺组织，癌前病变、原发癌及淋巴结转移癌组织中Star3、bcl-2和VEC-F的表达情况，并分析与各临床病理参数之间的关系。结果：实验组中Stat3、bcl-2、VEGF的表达阳性率分别为65．17％、77．53％、79．77％，均显著高于正常对照组（P〈0．05）；Stat3表达阳性率与组织学分级、临床分期及淋巴结转移有关（均P〈0．05）；肺癌中Stat3与VEGF，bcl-2的表达呈明显正相关。结论：Stat3与肺癌的浸润和转移密切相关，因而Stat3可用于判断肿瘤预后的指标检测。     

p53、MDM2、cyclin G在星形细胞瘤中的表达及与肿瘤分化和预后的关系

目的：分析p53、MDM2、cyclin G在星形细胞瘤中的表达及与肿瘤分化和预后的关系。方法：应用免疫组化S-P法对54例脑原发性星形细胞瘤中p53、MDM2、cyclin G的表达进行检测，对其中41例取得随访资料的肿瘤患者存活因素进行分析。结果：p53、MDM2表达在星形细胞瘤、间变型星形细胞瘤和多形性胶质母细胞瘤中差异有显著性（F=12．16，P〈0．01；F=1．89，P〈0．05）。星形细胞瘤中p53、MDM2、cyclin G表达率分别为61％、56％、63％。p53、MDM2、cyclin G表达标记指数随着肿瘤恶性程度的增加而逐渐增高。三者标记指数高的肿瘤预后差。结论：p53、MDM2、cyclin G过度表达与星形细胞瘤分化和预后密切相关，能够客观地反映肿瘤增生分化和恶性程度。可以作为判断星形细胞瘤分化和预后有价值的参考指标。     

VEGF、PCNA、MVD、flk-1在(人脑显形细胞瘤)中的表达及临床意义

目的 研究血管内皮细胞生长因子（vascular endothelial growth factor，VEGF）及其受体flk-1（fetal liver kinase-1）在人脑显形细胞瘤中的表达与肿瘤增殖及血管再生的相互关系。方法 应用免疫组化技术和形态定量分析法，检测69例手术切除脑胶质瘤中VEGF表达、PCNA标记指数（PCNAta）、微血管密度（Mierovessel density，MVD）及部分病例flk-1表达。结果（1）肿瘤细胞及血管内皮细胞均可以表达VEGF及flk-1，阳性颗粒分布于肿瘤胞浆中。（2）高级别肿瘤PCNALI、MVD显著高于低级别肿瘤（P〈0．05）；VEGF表达阳性肿瘤的PCNALI、MVD显著高于VEGF表达阴性肿瘤（P〈0．05）；（3）VEGF与其受体flk-1在肿瘤细胞中表达呈正相关；肿瘤组织VEGF及其受体flk-1表达与肿瘤的恶性程度呈正相关；（4）在星形细胞肿瘤中，随着MVD的增大，VEGF及flk-1在肿瘤血管内皮的染色率逐渐增加，分别与肿瘤的MVD存在正相关关系（r分别为0．40，0．44，P〈0．01）。结论 人脑显形细胞瘤可以合成VEGF，VEGF在肿瘤细胞增殖及血管再生过程中起重要作用。     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.     

Omi/HtrA2在窒息后血清诱导人近曲肾小管皮细胞凋亡中的作用

Objective To investigate the mechanism of inducing apoptosis of Omi/HtrA2 in renal tubular cells with postasphyxial serum of neonate. Methods Human renal proximal tubular cell line HK-2 cell was used as target cell. They were divided into three groups: control group, asphyxia group and Ucf-101 (Omi/HtrA2 special inhibitor) treated group. The challenge concentration of serum obtained from neonates 24 hours after asphyxia was 20%,and the treatment concentration of Ucf-101 was 10 μmol/L.The Omi/HtrA2 translocation in renal tubular cells was observed with confocal microscopy, and the rate of apoptosis was detected with flow cytometer. Results It was found that Omi/HtrA2 was translocated into cytoplasm in asphyxia group, and the rate of Omi/HtrA2 translocation in HK-2 cells of asphyxia group was significantly increased [(28. 1 % vs. (9.4±2.1)%, P<0. 01]. Compared with the control group, after being treated with postasphyxial serum, the rate of apoptosis of HK-2 cells in asphyxia group wa ssignificantly increased [(36. 3±4. 4)% vs. (12. 4±2. 9) %, P<0. 01]. Compared with asphyxia group, the rate of apoptosis in HK-2 cells in Ucf-101 treated group was significantly decreased [(27. 0± 3. 9)% vs. (36.3±4.4) %, P<0. 01]. Conclusion These experimental data demonstrates that postasphyxial serum of neonate can induce apoptosis of HK-2 cells, and translocation of Omi/HtrA2 from mitochondria into cyto-plasm may play an important role in its intracellular signal transduetion mechanism in induction of apoptosis.