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DI-3-n-butylphthalide exerts neuroprotective effects by modulating hypoxia-inducible factor 1-alpha ubiquitination to attenuate oxidative stress-induced apoptosis 被引量:9
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作者 Shuai Li Jingyuan Zhao +4 位作者 Yan Xi Jiaqi Ren Yanna Zhu Yan Lu Deshi Dong 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第11期2424-2428,共5页
DI-3-n-butylphthalide is used to treat mild and moderate acute ischemic stroke.However,the precise underlying mechanism requires further investigation.In this study,we investigated the molecular mechanism of DI-3-n-bu... DI-3-n-butylphthalide is used to treat mild and moderate acute ischemic stroke.However,the precise underlying mechanism requires further investigation.In this study,we investigated the molecular mechanism of DI-3-n-butylphthalide action by various means.We used hydrogen peroxide to induce injury to PC12cells and RAW264.7 cells to mimic neuronal oxidative stress injury in stroke in vitro and examined the effects of DI-3-n-butylphthalide.We found that DI-3-nbutylphthalide pretreatment markedly inhibited the reduction in viability and reactive oxygen species production in PC12 cells caused by hydrogen peroxide and inhibited cell apoptosis.Furthermore,DI-3-n-butylphthalide pretreatment inhibited the expression of the pro-apoptotic genes Bax and Bnip3.DI-3-nbutylphthalide also promoted ubiquitination and degradation of hypoxia inducible factor 1α,the key transcription factor that regulates Bax and Bnip3 genes.These findings suggest that DI-3-n-butylphthalide exhibits a neuroprotective effect on stroke by promoting hypoxia inducible factor-1α ubiquitination and degradation and inhibiting cell apoptosis. 展开更多
关键词 blood-brain barrier Dl-3-n-butylphthalide hypoxia inducible factor MITOCHONDRIA NEUROPROTECTION oxidative stress reactive oxygen species stroke transcription factor UBIQUITINATION
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Hypoxia upregulates hypoxia inducible factor(HIF)-3α expression in lung epithelial cells: characterization and comparison with HIF-1α 被引量:16
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作者 Qi Fang Li Xiang Rui Wang Yue Wu Yang Han Lin 《Cell Research》 SCIE CAS CSCD 2006年第6期548-558,共11页
The role of the hypoxia-inducible factor(HIF)subunits 1α and 2α in response to hypoxia is well established in lungepithelial cells,whereas little is known about HIF-3α with respect to transcriptional and translatio... The role of the hypoxia-inducible factor(HIF)subunits 1α and 2α in response to hypoxia is well established in lungepithelial cells,whereas little is known about HIF-3α with respect to transcriptional and translational regulation by hy-poxia.HIF-3α and HIF-1α are two similar but distinct basic helix-loop-helix-PAS proteins,which have been postulatedto activate hypoxia responsive genes in response to hypoxia.Here,we used quantitative real time RT-PCR and immu-noblotting to determine the activation of HIF-3α vs.HIF-1α by hypoxia.HIF-3α was strongly induced by hypoxia(1%O_2)both at the level of protein and mRNA due to an increase in protein stability and transcriptional activation,whereasHIF-1α protein and mRNA levels enhanced transiently and then decreased because of a reduction in its mRNA stabilityin A549 cells,as measured on mRNA and protein levels.Interestingly,HIF-3α and HIF-1α exhibited strikingly similarresponses to a variety of activating or inhibitory pharmacological agents.These results demonstrate that HIF-3α is ex-pressed abundantly in lung epithelial cells,and that the transcriptional induction of HIF-3α plays an important role in theresponse to hypoxia in vitro.Our findings suggest that HIF-3α,as a member of the HIF system,is complementary ratherthan redundant to HIF-1α induction in protection against hypoxic damage in alveolar epithelial cells. 展开更多
关键词 hypoxia inducible factor alveolar epithelial type cells hypoxia gene expression in vitro
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Low hypoxia inducible factor-1α(HIF-1α)expression in testicular germ cell tumors--a major reason for enhanced chemosensitivity? 被引量:5
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作者 niraj shenoy roxana dronca +6 位作者 fernando quevedo stephen a boorjian john cheville brian costello manish kohli thomas witzig lance pagliaro 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2017年第4期374-378,共5页
The molecular basis for enhanced chemosensitivity of testicular germ cell tumors (GCT) has been an area of great interest, as it could potentially give us therapeutic leads in other resistant malignancies. Thus far,... The molecular basis for enhanced chemosensitivity of testicular germ cell tumors (GCT) has been an area of great interest, as it could potentially give us therapeutic leads in other resistant malignancies. Thus far, however, the increased sensitivity of C&T has been variously attributed to multiple factors -- an inability to detoxify cisplatin, a lack of export pumps, an inability to repair the DNA damage, an intact apoptotic cascade and lack of p53 mutation; but a unifying underlying etiology leading to the aforementioned processes and having a translational implication has so far been elusive. Herein, we offer evidence to support a potential significant role for the previously demonstrated low hypoxia inducible factor-la (HIF-la) expression in mediating the general exquisite chemosensitivity of testicular GCT, through the aforementioned processes. This molecular mechanism based hypothesis could have a significant translational implication in platinum refractory GCT as well as other platinum resistant malignancies. 展开更多
关键词 hypoxia inducible factor-la hif-la) testicular germ cell tumor CHEMOSENSITIVITY
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Metabolic shift in liver: Correlation between perfusion temperature and hypoxia inducible factor-1α 被引量:5
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作者 Andrea Ferrigno Laura Giuseppina Di Pasqua +2 位作者 Alberto Bianchi Plinio Richelmi Mariapia VairettiAndrea Ferrigno 《World Journal of Gastroenterology》 SCIE CAS 2015年第4期1108-1116,共9页
AIM: To study at what temperature the oxygen carried by the perfusate meets liver requirements in a model of organ perfusion. METHODS: in this study, we correlated hypoxia induciblefactor(Hi F)-1α expression to the p... AIM: To study at what temperature the oxygen carried by the perfusate meets liver requirements in a model of organ perfusion. METHODS: in this study, we correlated hypoxia induciblefactor(Hi F)-1α expression to the perfusion temperature and the hepatic oxygen uptake in a model of isolated perfused rat liver. Livers from Wistar rats were perfused for 6 h with an oxygenated medium at 10, 20, 30 and 37 ℃. Oxygen uptake was measured by an oxygen probe; lactate dehydrogenase activity, lactate release and glycogen were measured spectrophotometrically; bile flow was gravitationally determined; p H of the perfusate was also evaluated; Hi F-1α m RNA and protein expression were analyzed by real time-polymerase chain reaction and ELi SA, respectively. RESULTS: Livers perfused at 10 and 20 ℃ showed no difference in lactate dehydrogenase release after 6 h of perfusion(0.96 ± 0.23 vs 0.93 ± 0.09 m U/min per g) and had lower hepatic damage as compared to 30 and 37 ℃(5.63 ± 0.76 vs 527.69 ± 45.27 m U/min per g, respectively, P s < 0.01). After 6 h, tissue ATP was significantly higher in livers perfused at 10 and 20 ℃than in livers perfused at 30 and 37 ℃(0.89 ± 0.06 and 1.16 ± 0.05 vs 0.57 ± 0.09 and 0.33 ± 0.08 nmol/mg, respectively, P s < 0.01). No sign of hypoxia was observed at 10 and 20 ℃, as highlighted by low lactate release respect to livers perfused at 30 and 37 ℃(121.4 ± 12.6 and 146.3 ± 7.3 vs 281.8 ± 45.3 and 1094.5 ± 71.7 nmol/m L, respectively, P s < 0.02), and low relative Hi F-1α m RNA(0.40 ± 0.08 and 0.20 ± 0.03 vs 0.60 ± 0.20 and 1.47 ± 0.30, respectively, P s < 0.05) and protein(3.72 ± 0.16 and 3.65 ± 0.06 vs 4.43 ± 0.41 and 6.44 ± 0.82, respectively, P s < 0.05) expression.CONCLUSION: Livers perfused at 10 and 20 ℃ show no sign of liver injury or anaerobiosis, in contrast to livers perfused at 30 and 37 ℃. 展开更多
关键词 ANAEROBIOSIS hypoxia inducible factor-1 α ISCHEMIA
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Desferoxamine preconditioning protects against cerebral ischemia in rats by inducing expressions of hypoxia inducible factor 1α and erythropoietin 被引量:1
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作者 李云霞 丁素菊 +2 位作者 肖林 郭卫 詹青 《Neuroscience Bulletin》 SCIE CAS CSCD 2008年第2期89-95,共7页
Objective To investigate whether desferoxamine (DFO) preconditioning can induce tolerance against cerebral ischemia and its effect on the expression of hypoxia inducible factor 1 α (HIF- 1α) and erythropoietin ... Objective To investigate whether desferoxamine (DFO) preconditioning can induce tolerance against cerebral ischemia and its effect on the expression of hypoxia inducible factor 1 α (HIF- 1α) and erythropoietin (EPO) in vivo and in vitro. Methods Rat model of cerebral ischemia was established by middle cerebral artery occlusion with or without DFO administration. Infarct size was examined by TTC staining, and the neurological severity score was evaluated according to published method. Cortical neurons were cultured under ischemia stress which was mimicked by oxygen-glucose deprivation (OGD), and the neuron damage was assessed by MTT assay. Immunofluorescent staining was employed to detect the expressions of HIF-1 and EPO. Results The protective effect induced by DFO (decreasing the infarction volume and ameliorating the neurological function) appeared at 2 d after administration ofDFO (post-DFO), lasted until 7 d and disappeared at 14 d (P 〈 0.05); the most effective action was observed at 3 d post-DFO. DFO induced tolerance of cultured neurons against OGD: neuronal viability was increased 23%, 34%, 40%, 48% and 56% at 8 h, 12 h, 24 h, 36 h, and 48 h, respectively, post-DFO (P 〈 0.05). Immunofluorescent staining found that HIF-1 α and EPO were upregulated in the neurons of rat brain at 3 d and 7 d post-DFO; increase of HIF-1 α and EPO appeared in cultured cortex neurons at 36 h and 48 h post-DFO. Conclusion DFO induced tolerance against focal cerebral ischemia in rats, and exerted protective effect on OGD cultured cortical neurons. DFO significant induced the expression of HIF- 1 α and EPO both in vivo and in vitro. DFO preconditioning can protect against cerebral ischemia, which may be associated with the synthesis of HIF- 1 α and EPO. 展开更多
关键词 desferoxamine ischemia preconditioning hypoxia inducible factor 1 α ERYTHROPOIETIN
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胎儿生长受限患者胎盘组织中VEGFA、HIF-1α表达及临床意义
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作者 王宏艳 徐志文 +2 位作者 孙晓东 朱秀民 崔元日 《中国计划生育学杂志》 2024年第7期1663-1667,1672,共6页
目的:探究胎儿生长受限(FGR)患者胎盘组织中血管内皮生长因子A(VEGFA)、缺氧诱导因子(HIF)-1α表达及临床意义。方法:选择2020年5月-2022年9月在本院确诊FGR并住院分娩的孕妇116例(FGR组)、分娩正常孕妇(新生儿正常)116例为对照组临床... 目的:探究胎儿生长受限(FGR)患者胎盘组织中血管内皮生长因子A(VEGFA)、缺氧诱导因子(HIF)-1α表达及临床意义。方法:选择2020年5月-2022年9月在本院确诊FGR并住院分娩的孕妇116例(FGR组)、分娩正常孕妇(新生儿正常)116例为对照组临床资料。qRT-PCR检测胎盘组织中VEGFA、HIF-1α的mRNA表达情况,免疫组化法检测VEGFA、HIF-1α的蛋白表达情况。Pearson相关性分析VEGFA与HIF-1α的相关性以及与FGR患者临床资料相关性;多因素logistic回归分析影响FGR发生的因素。结果:FGR组VEGFA蛋白阳性表达率(25.9%)低于对照组(64.7%),HIF-1α蛋白阳性表达率(67.2%)高于对照组(24.1%);FGR组胎盘组织中VEGFA mRNA表达水平(0.75±0.20)低于对照组(1.00±0.23),HIF-1α mRNA表达水平(1.26±0.25)高于对照组(1.01±0.19)(均P<0.05)。FGR患者胎盘组织中VEGFA mRNA与HIF-1α mRNA呈负相关(P<0.05)。FGR患者新生儿出生1 min Apgar评分、胎盘重量、胎盘体积、新生儿体重与VEGFA表达水平呈正相关,与HIF-1α表达水平呈负相关;HIF-1α升高为影响FGR发生的危险因素,VEGFA升高为保护因素(均P<0.05)。结论:FGR患者胎盘组织中VEGFA低表达、HIF-1α高表达,二者影响FGR的发生及新生儿出生质量。 展开更多
关键词 胎儿生长受限 胎盘组织 血管内皮生长因子A 缺氧诱导因子-1Α 相关性 影响因素 新生儿
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瑞马唑仑调节HIF-1α/BNIP3信号通路对OGD/R诱导神经细胞自噬和凋亡的影响
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作者 王效德 后晓超 +3 位作者 李青青 司玉婷 周小平 徐桂萍 《河北医药》 CAS 2024年第8期1138-1141,1146,共5页
目的探讨瑞马唑仑对OGD/R诱导的神经细胞自噬和凋亡的影响及作用机制。方法体外培养小鼠海马神经元细胞(HT22)并进行神经细胞氧糖剥夺/再复氧(OGD/R),筛选实验用瑞马唑仑浓度;将HT22细胞分为对照组、OGD/R组、瑞马唑仑组、2-ME2组、瑞... 目的探讨瑞马唑仑对OGD/R诱导的神经细胞自噬和凋亡的影响及作用机制。方法体外培养小鼠海马神经元细胞(HT22)并进行神经细胞氧糖剥夺/再复氧(OGD/R),筛选实验用瑞马唑仑浓度;将HT22细胞分为对照组、OGD/R组、瑞马唑仑组、2-ME2组、瑞马唑仑+2-ME2组;CCK8法检测5组HT22细胞活力;流式细胞术检测5组HT22细胞凋亡率;透射电子显微镜观察5组HT22细胞自噬小体的形成;Western blot检测5组HT22细胞HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ的表达。结果确定实验用瑞马唑仑浓度为50μg/mL;与对照组比较,OGD/R组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05);与OGD/R组比较,瑞马唑仑组HT22细胞自噬小体增加,OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平上调,凋亡率下调(P<0.05);2-ME2组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05)。与瑞马唑仑组比较,瑞马唑仑+2-ME2组HT22细胞自噬小体数量减少,OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平下调,凋亡率上调(P<0.05);与2-ME2组比较,瑞马唑仑+2-ME2组HT22细胞OD450值、HIF-1α、BNIP3、LC3-Ⅱ/LC3-Ⅰ蛋白水平上调,凋亡率下调(P<0.05)。结论瑞马唑仑可通过激活HIF-1α/BNIP3信号通路促进OGD/R诱导的神经细胞自噬,抑制细胞凋亡,从而减轻OGD/R诱导的神经细胞损伤。 展开更多
关键词 瑞马唑仑 hif-1α/BNIP3信号通路 OGD/R诱导的神经细胞 自噬 凋亡
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血清HIF-1α、NSE、GFAP及相关临床特征与新生儿缺氧缺血性脑病发生风险的关系分析
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作者 李晶晶 卢志华 +2 位作者 王可可 吴超君 李巍 《中国现代医学杂志》 CAS 2024年第7期73-78,共6页
目的探讨血清低氧诱导因子-1α(HIF-1α)、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)及相关临床特征与新生儿缺氧缺血性脑病(HIE)发生风险的关系。方法选取2020年1月—2023年1月苏州大学附属儿童医院收治的85例HIE患儿作为HIE... 目的探讨血清低氧诱导因子-1α(HIF-1α)、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)及相关临床特征与新生儿缺氧缺血性脑病(HIE)发生风险的关系。方法选取2020年1月—2023年1月苏州大学附属儿童医院收治的85例HIE患儿作为HIE组,另选取同期在该院出生的120例健康新生儿作为对照组,分析两组的临床资料并检测新生儿出生后3 d血清HIF-1α、NSE、GFAP水平。绘制受试者工作特征(ROC)曲线分析血清HIF-1α、NSE、GFAP水平预测新生儿HIE发病的价值;多因素逐步Logistic回归模型分析新生儿HIE发病的影响因素。结果与对照组相比,HIE组宫内窘迫、脐带异常、羊水污染、1 min Apgar评分≤7分的患儿比例较高(P<0.05),并且血清HIF-1α、NSE、GFAP水平较高(P<0.05);两组孕妇年龄、孕妇文化程度、胎龄、新生儿性别、出生体重、产次、剖宫产、胎膜早破比较,差异均无统计学意义(P>0.05)。ROC曲线分析结果显示,HIF-1α、NSE、GFAP及三者联合预测新生儿HIE发病的敏感性分别为82.7%(95%CI:0.795,0.862)、78.7%(95%CI:0.705,0.849)、84.0%(95%CI:0.803,0.891)、85.3%(95%CI:0.788,0.922),特异性分别为85.3%(95%CI:0.816,0.907)、74.7%(95%CI:0.715,0.796)、72.0%(95%CI:0.692,0.771)、90.5%(95%CI:0.825,0.956),AUC分别为0.907(95%CI:0.884,0.930)、0.850(95%CI:0.816,0.884)、0.893(95%CI:0.827,0.959)、0.936(95%CI:0.905,0.967);多因素逐步Logistic回归分析显示,宫内窘迫[O^R=3.592(95%CI:2.017,6.397)]、脐带异常[O^R=4.905(95%CI:2.862,8.406)]、羊水污染[O^R=7.262(95%CI:3.603,14.637)]、1 min Apgar评分≤7分[O^R=3.139(95%CI:1.954,5.043)]、HIF-1α≥0.463 ng/mL[O^R=2.916(95%CI:1.422,5.980)]、NSE≥12.395μg/L[O^R=3.714(95%CI:1.955,7.056)]、GFAP≥3.962 ng/mL[O^R=3.556(95%CI:2.039,6.202)]均是新生儿HIE发病的危险因素(P<0.05)。结论宫内窘迫、脐带异常、羊水污染、出生后1 min Apgar评分低及血清HIF-1α、NSE、GFAP水平高是新生儿HIE发病的危险因素,临床通过检测血清HIF-1α、NSE、GFAP水平可为临床筛查HIE提供帮助,3项指标联合检测可进一步提高诊断价值。 展开更多
关键词 缺氧缺血性脑病 新生儿 临床特征 低氧诱导因子-1Α 神经元特异性烯醇化酶 胶质纤维酸性蛋白
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TSLP、HIF-1α、RANKL在义齿修复后种植体周围炎患者龈沟液中的表达及意义
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作者 张云霞 杨娜 +2 位作者 姚莉 符建青 王全智 《临床和实验医学杂志》 2024年第15期1656-1659,共4页
目的研究胸腺基质淋巴细胞生成素(TSLP)、缺氧诱导因子1α(HIF-1α)、核因子-κB受体活化因子配体(RANKL)在义齿修复后种植体周围炎(PI)患者龈沟液中的表达及意义。方法回顾性选取2019年8月至2023年8月大同市第五人民医院收治的义齿修... 目的研究胸腺基质淋巴细胞生成素(TSLP)、缺氧诱导因子1α(HIF-1α)、核因子-κB受体活化因子配体(RANKL)在义齿修复后种植体周围炎(PI)患者龈沟液中的表达及意义。方法回顾性选取2019年8月至2023年8月大同市第五人民医院收治的义齿修复患者86例作为研究对象,根据术后3个月是否发生PI将患者分为预后良好组(n=61)和预后不良组(n=25)。比较两组患者的临床资料及术前龈沟液TSLP、HIF-1α及RANKL水平,采用多因素Logistic回归分析对龈沟液TSLP、HIF-1α及RANKL水平与义齿修复患者术后发生PI的关系进行分析,采用受试者操作特征(ROC)曲线分析TSLP、HIF-1α及RANKL水平对义齿修复患者的预后评估价值。结果两组患者临床资料(性别、年龄、病程、义齿种植原因及种植颗数)比较,差异均无统计学意义(P>0.05)。预后良好组患者的龈沟液中TSLP、HIF-1α、RANKL水平分别为(122.57±11.30)ng/L、(417.79±115.43)ng/mL、(116.02±13.45)pg/μL,均明显低于预后不良组[(138.93±12.70)ng/L、(576.55±177.60)ng/mL、(133.24±15.69)pg/μL],差异均有统计学意义(P<0.05)。Logistic回归分析义齿修复患者预后,结果显示龈沟液中TSLP水平升高、HIF-1α水平升高和RANKL水平升高是义齿修复患者术后发生PI的独立危险因素(OR=1.119,95%CI:1.048~1.195;OR=1.007,95%CI:1.002~1.013;OR=1.065,95%CI:1.016~1.117;P<0.05)。ROC曲线分析龈沟液中TSLP、HIF-1α、RANKL水平预测义齿修复患者预后的价值,结果显示曲线下面积(AUC)值分别为0.833、0.786和0.809。其中,RANKL具有最高的特异度(0.852),而HIF-1α具有最高的敏感度(0.800),具有较好的预测价值(P<0.05)。结论龈沟液中TSLP、HIF-1α、RANKL水平升高是义齿修复患者术后并发PI的独立危险因素,且均具有较高的预测义齿修复患者预后的价值。 展开更多
关键词 义齿修复术 牙种植体 缺氧诱导因子1 α亚基 胸腺基质淋巴细胞生成素 核因子-ΚB受体活化因子配体 种植体周围炎 龈沟液
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乳腺癌组织内VEGF-C、HIF-1α表达与血管生成的相关性研究
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作者 刘焱 宋璐 林敏 《中外医学研究》 2024年第28期73-77,共5页
目的:探讨乳腺癌患者组织内血管内皮生长因子-C(VEGF-C)、缺氧诱导因子-1α(HIF-1α)表达与血管生成的关系。方法:选取2022年1月—2023年12月泰安市中心医院收治的198例乳腺癌女性患者,并选取同期经病理学检查为乳腺纤维瘤患者50例为对... 目的:探讨乳腺癌患者组织内血管内皮生长因子-C(VEGF-C)、缺氧诱导因子-1α(HIF-1α)表达与血管生成的关系。方法:选取2022年1月—2023年12月泰安市中心医院收治的198例乳腺癌女性患者,并选取同期经病理学检查为乳腺纤维瘤患者50例为对照。采用免疫组化S-P法检测乳腺癌和乳腺纤维瘤组织中VEGF-C、HIF-1α表达及微血管密度(MVD)数,分析VEGF-C、HIF-1α表达与临床病理特征及MVD的关系。结果:乳腺癌患者乳腺组织中VEGF-C、HIF-1α阳性表达率及MVD数均高于乳腺纤维瘤患者,差异有统计学意义(P<0.05)。VEGF-C阳性与阴性表达者年龄、肿瘤直径、组织学分级、ER表达、PR表达等临床病理特征比较,差异无统计学意义(P>0.05);VEGF-C阳性表达者有淋巴结转移、TNM分期为Ⅲ~Ⅳ期、分子分型(Luminal B、HER-2阳性、基底细胞)的患者占比及MVD均高于VEGF-C阴性表达者,差异有统计学意义(P<0.05)。HIF-1α阳性与阴性表达者年龄、肿瘤直径、ER表达、PR表达、分子分型等临床病理特征比较,差异无统计学意义(P>0.05);HIF-1α阳性表达者组织学分级为Ⅱ级、Ⅲ级、有淋巴结转移、TNM分期为Ⅲ~Ⅳ期的患者占比及MVD均高于HIF-1α阴性表达者,差异有统计学意义(P<0.05)。结论:乳腺癌患者组织内VEGF-C、HIF-1α阳性表达率明显升高,并且还与肿瘤血管生成存在显著相关性。 展开更多
关键词 乳腺癌 血管内皮生长因子 -C 缺氧诱导因子 -1α 临床病理特征 微血管密度
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CD133、HER2、HIF-1α在胃癌组织中的表达及与患者Hp感染、淋巴结转移和预后的关系分析 被引量:1
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作者 金欢 许晴晴 薛晓婕 《临床和实验医学杂志》 2024年第1期16-20,共5页
目的探究中性粒细胞表面抗原(CD133)、人类表皮生长因子受体2(HER2)、缺氧诱导因子-1α(HIF-1α)在胃癌组织中的表达及与患者幽门螺杆菌(Hp)感染、淋巴结转移和预后的关系。方法回顾性选取2020年1月至2021年1月在黄石市中心医院/湖北理... 目的探究中性粒细胞表面抗原(CD133)、人类表皮生长因子受体2(HER2)、缺氧诱导因子-1α(HIF-1α)在胃癌组织中的表达及与患者幽门螺杆菌(Hp)感染、淋巴结转移和预后的关系。方法回顾性选取2020年1月至2021年1月在黄石市中心医院/湖北理工学院附属医院进行治疗的100例胃癌患者作为研究对象。所有患者中,存在Hp感染75例,未发生Hp感染25例;存在淋巴结转移45例,未发生淋巴结转移55例。随访2年,56例患者发生复发或死亡,纳入预后不良组,其余44例纳入预后良好组。取患者的胃癌组织及癌旁组织,对组织中CD133、HER2、HIF-1α表达情况进行比较,并探究CD133、HER2、HIF-1α表达情况与患者Hp感染、淋巴结转移和预后的关系,并采用受试者工作特征(ROC)曲线分析CD133、HER2、HIF-1α表达对预后不良的预测价值。结果胃癌组织中CD133、HER2、HIF-1α表达阳性率分别为81.00%、25.00%、66.00%,均高于癌旁组织(18.00%、4.00%、44.00%),差异均有统计学意义(P<0.05)。发生Hp感染的患者中胃癌组织的CD133、HER2、HIF-1α表达阳性率分别为74.67%、30.67%、72.00%,均显著高于未发生Hp感染患者(48.00%、8.00%、48.00%),差异均有统计学意义(P<0.05)。淋巴结转移患者胃癌组织的CD133、HER2、HIF-1α表达阳性率分别为93.33%、48.89%、80.00%,均高于未发生淋巴结转移患者(70.91%、5.45%、54.55%),差异均有统计学意义(P<0.05)。预后不良组患者胃癌组织的CD133、HER2、HIF-1α表达阳性率分别为83.93%、37.50%、75.00%,均显著高于预后良好组患者(47.73%、9.09%、54.55%),差异均有统计学意义(P<0.05)。ROC曲线结果显示,CD133、HER2表达阳性率对胃癌预后不良的预测曲线下面积(AUC)值分别为0.781、0.762,HIF-1α表达阳性率对胃癌预后不良的预测AUC值为0.602。结论CD133、HER2、HIF-1α在胃癌组织及发生感染Hp、淋巴结转移患者中存在高表达,且CD133、HER2表达对患者预后有一定预测价值。 展开更多
关键词 受体 人类表皮生长因子 缺氧诱导因子 Α亚基 中性粒细胞表面抗原 胃癌 幽门螺杆菌 淋巴结转移
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落新妇苷通过调节HIF-1α/VEGF轴抑制乳腺癌细胞的增殖、迁移和血管生成拟态形成
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作者 王媛媛 顾玉 +2 位作者 刘秋霞 马胜辉 龚志平 《中国肿瘤生物治疗杂志》 CAS CSCD 北大核心 2024年第8期796-802,共7页
目的:探究落新妇苷(AST)调节低氧诱导因子-1α(HIF-1α)/血管内皮生长因子(VEGF)轴对乳腺癌细胞增殖、迁移和血管生成拟态(VM)的影响。方法:用不同浓度的AST(0、5、25、50、100、150、200、300μmol/L)处理乳腺癌细胞MCF-7、MDA-MB-231... 目的:探究落新妇苷(AST)调节低氧诱导因子-1α(HIF-1α)/血管内皮生长因子(VEGF)轴对乳腺癌细胞增殖、迁移和血管生成拟态(VM)的影响。方法:用不同浓度的AST(0、5、25、50、100、150、200、300μmol/L)处理乳腺癌细胞MCF-7、MDA-MB-231,采用CKK-8法检测细胞活力。将MCF-7、MDA-MB-231细胞分为对照组、AST低剂量(AST-L)组、AST中剂量(AST-M)、AST高剂量(AST-H)组、AST-H+DMOG(HIF-1α/VEGF通路激活剂)组,EdU法检测AST处理对乳腺癌细胞增殖的影响,流式细胞术检测其对细胞凋亡的影响,Transwell小室实验检测其对细胞迁移、侵袭能力的影响,Matrigel管型形成实验检测其对细胞VM形成的影响,WB法检测对细胞中HIF-1α、VEGF、VE-cadherin、E-cadherin、N-cadherin、MMP-2表达的影响。结果:与0μmol/L AST相比,5、25、50、100、150、200、300μmol/L AST处理的细胞活力显著下降,呈剂量依赖性(P<0.05)。与对照组相比,AST-L、AST-M、AST-H组细胞EdU阳性率、细胞迁移数、细胞侵袭数、VM管腔数目、HIF-1α、VEGF、VE-cadherin、N-cadherin、MMP-2表达均显著下降,而细胞凋亡率、E-cadherin蛋白表达显著升高(均P<0.05);与AST-H组相比,AST-H+DMOG组细胞EdU阳性率、细胞迁移数、细胞侵袭数、VM管腔数目、HIF-1α、VEGF、VE-cadherin、N-cadherin、MMP-2表达均显著升高,而细胞凋亡率、E-cadherin蛋白表达均显著下降(均P<0.05)。结论:AST能抑制乳腺癌细胞增殖、迁移、侵袭和VM形成,促进凋亡,其作用机制可能与抑制HIF-1α/VEGF信号通路有关。 展开更多
关键词 乳腺癌 落新妇苷 增殖 迁移 血管生成拟态 低氧诱导因子-1α/血管内皮生长因子
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Expression of Nerve Growth Factor and Hypoxia Inducible Factor-1α and Its Correlation with Angiogenesis in Non-Small Cell Lung Cancer 被引量:8
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作者 逯青丽 刘建 +1 位作者 朱晓莉 徐文佳 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2014年第3期359-362,共4页
Summary: In order to investigate the expression of nerve growth factor (NGF) and hypoxia inducible factor-1α (HIF-1α) and its correlation with angiogenesis in non-small cell lung cancer (NSCLC), paraffin-embe... Summary: In order to investigate the expression of nerve growth factor (NGF) and hypoxia inducible factor-1α (HIF-1α) and its correlation with angiogenesis in non-small cell lung cancer (NSCLC), paraffin-embedded tissue blocks from 20 patients with NSCLC were examined. Twenty corresponding para-cancerous lung tissue specimens were obtained to serve as a control. The expression of NGF, HIF-1α, and vascular endothelial growth factor (VEGF) in the NSCLC tissues was detected by using immunohistochemistry. The microvascular density (MVD) was determined by CD31 staining. The resuits showed that the expression levels ofNGF, HIF-1α and VEGF in the NSCLC tissues were remarkably higher than those in the para-cancerous lung tissues (P〈0.05). There was significant difference in the MVD between the NSCLC tissues (9.19±1.43) and para-cancerous lung tissues (2.23±1.19) (P〈0.05). There were positive correlations between NGF and VEGF, between HIF-1α and VEGF, and between NGF and HIF-1α in NSCLC tissues, with the spearman correlation coefficient being 0.588, 0.519 and 0.588, respectively. In NSCLC tissues, the MVD had a positive correlation with the three factors (P〈0.05). Theses results suggest that NGF and HIF-1α are synergically involved in the angiogenesis of NSCLC. 展开更多
关键词 non-small cell lung cancer IMMUNOHISTOCHEMISTRY nerve growth factor hypoxia inducible factor-1α vascular endothelial growth factor CD31 microvascular density
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紫草素调节HIF-1α/NLRP3信号通路对蛛网膜下腔出血大鼠神经功能损伤的影响
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作者 饶重贤 胡姗姗 +3 位作者 谭伟 王军民 金胜昔 周游 《河北医药》 CAS 2024年第4期496-500,505,共6页
目的探究紫草素调节缺氧诱导因子-1α(HIF-1α)/NOD样受体热蛋白结构域相关蛋白3(NLRP3)信号通路对蛛网膜下腔出血(SAH)大鼠神经功能损伤的影响。方法大鼠随机分为假手术组、模型组、YC-1(HIF-1α抑制剂,5 mg/kg)组、紫草素低剂量组(4 m... 目的探究紫草素调节缺氧诱导因子-1α(HIF-1α)/NOD样受体热蛋白结构域相关蛋白3(NLRP3)信号通路对蛛网膜下腔出血(SAH)大鼠神经功能损伤的影响。方法大鼠随机分为假手术组、模型组、YC-1(HIF-1α抑制剂,5 mg/kg)组、紫草素低剂量组(4 mg/kg)、紫草素高剂量组(25 mg/kg)、紫草素高剂量(25 mg/kg)+AG1(HIF-1α激活剂,10 mg/kg)组,每组15只。采用颈内动脉刺破法制备SAH模型。采用Zea-Longa评分法评估6组大鼠神经功能;ELISA法检测血清肿瘤坏死因子α(TNF-α)、白介素-6(IL-6)和IL-1β水平;HE染色观察大鼠海马组织形态学变化,TUNEL染色法检测海马神经元凋亡率;伊文思蓝染色检测血脑屏障通透性;商品化试剂盒检测大鼠脑组织超氧化物歧化酶(SOD)、过氧化氢酶(MDA)、丙二醛(CAT)水平,Western blot检测大鼠脑组织Bax、Bcl-2、HIF-1α、NLRP3蛋白表达。结果假手术组大鼠海马神经元形态结构正常;与假手术组相比,模型组大鼠海马神经元有大量水肿、结构模糊,有细胞核溶解,变型固缩,部分细胞核消失,大鼠神经功能评分、血清TNF-α、IL-6和IL-1β水平、海马神经元凋亡率、伊文思蓝渗出量、脑组织MDA水平、Bax、HIF-1α、NLRP3水平显著增加,脑组织SOD、CAT水平、Bcl-2蛋白水平显著降低(P<0.05);与模型组比较,紫草素低剂量组、紫草素高剂量组和YC-1组鼠海马神经元病理损伤显著改善,大鼠神经功能评分、血清TNF-α、IL-6和IL-1β水平、海马神经元凋亡率、伊文思蓝渗出量、脑组织MDA水平、Bax、HIF-1α、NLRP3水平显著降低,SOD、CAT水平、Bcl-2蛋白水平显著升高(P<0.05);与紫草素高剂量组比较,紫草素高剂量+AG1组大鼠海马神经元病理损伤显著加重,大鼠神经功能评分、血清TNF-α、IL-6和IL-1β水平、海马神经元凋亡率、伊文思蓝渗出量、脑组织MDA水平、Bax、HIF-1α、NLRP3水平显著增加,SOD、CAT水平、Bcl-2蛋白水平显著降低(P<0.05)。结论紫草素抑制HIF-1α/NLRP3信号通路以降低氧化应激和炎性反应,进而改善SAH大鼠神经功能损伤。 展开更多
关键词 紫草素 hif-1α/NLRP3信号通路 蛛网膜下腔出血 神经功能损伤
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Activation of hypoxia-inducible factor 1 attenuates periapical inflammation and bone loss 被引量:22
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作者 Kimito Hirai Hisako Furusho +1 位作者 Kiichi Hirota Hajime Sasaki 《International Journal of Oral Science》 SCIE CAS CSCD 2018年第2期92-101,共10页
Hypoxia(low oxygen level) is an important feature during infections and affects the host defence mechanisms. The host has evolved specific responses to address hypoxia, which are strongly dependent on the activation... Hypoxia(low oxygen level) is an important feature during infections and affects the host defence mechanisms. The host has evolved specific responses to address hypoxia, which are strongly dependent on the activation of hypoxia-inducible factor 1(HIF-1).Hypoxia interferes degradation of HIF-1 alpha subunit(HIF-1α), leading to stabilisation of HIF-1α, heterodimerization with HIF-1 beta subunit(HIF-1β) and subsequent activation of HIF-1 pathway. Apical periodontitis(periapical lesion) is a consequence of endodontic infection and ultimately results in destruction of tooth-supporting tissue, including alveolar bone. Thus far, the role of HIF-1 in periapical lesions has not been systematically examined. In the present study, we determined the role of HIF-1 in a wellcharacterised mouse periapical lesion model using two HIF-1α-activating strategies, dimethyloxalylglycine(DMOG) and adenovirusinduced constitutively active HIF-1α(CA-HIF1 A). Both DMOG and CA-HIF1 A attenuated periapical inflammation and tissue destruction. The attenuation in vivo was associated with downregulation of nuclear factor-κappa B(NF-κB) and osteoclastic gene expressions. These two agents also suppressed NF-κB activation and subsequent production of proinflammatory cytokines by macrophages. Furthermore, activation of HIF-1α by DMOG specifically suppressed lipopolysaccharide-stimulated macrophage differentiation into M1 cells, increasing the ratio of M2 macrophages against M1 cells. Taken together, our data indicated that activation of HIF-1 plays a protective role in the development of apical periodontitis via downregulation of NF-κB, proinflammatory cytokines, M1 macrophages and osteoclastogenesis. 展开更多
关键词 CA Activation hypoxia-inducible factor attenuates periapical inflammation bone loss hif
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Hypoxia inducible factor in hepatocellular carcinoma:A therapeutic target 被引量:23
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作者 Daniel Lin Jennifer Wu 《World Journal of Gastroenterology》 SCIE CAS 2015年第42期12171-12178,共8页
Hepatocellular carcinoma(HCC) is one of the most commonly diagnosed and deadly cancers worldwide; its incidence has been rising in the United States due to the increase in hepatitis C associated cirrhosis and the grow... Hepatocellular carcinoma(HCC) is one of the most commonly diagnosed and deadly cancers worldwide; its incidence has been rising in the United States due to the increase in hepatitis C associated cirrhosis and the growing epidemic of obesity. There have been no effective therapeutic options in the advanced disease setting beyond sorafenib, a multi-targeted tyrosine kinase inhibitor that showed significant survival benefit. Because of this, there is an urgent need to search for novel pathways in sorafenib experienced patients. This review will focus on the role of hypoxia and hypoxiainducible factor alpha(HIF-1α) in cancer development, specifically in HCC. We will discuss the biology of HIF-1α, the pathways with which it interacts, and the function of HIF-1α in HCC. Furthermore, we will review studies highlighting the relevance of HIF-1α in the clinical setting, as well as the pre-clinical data supporting its further investigation. Finally, we will conclude with a discussion of the potential role of a HIF-1α m RNA antagonist for the treatment of HCC, and hypothesize the ways in which such an inhibitor may be best utilized in the management of advanced HCC. Hypoxia plays a significant role in the development of HCC. HIF-1α is a key transcription factor involved in the hypoxic response of cancer cells. It activates transcription of genes responsible for angiogenesis, glucose metabolism, proliferation, invasion and metastasis in HCC. Its involvement in multiple, essential tumor pathways makes it an attractive potential therapeutic target in HCC. 展开更多
关键词 hypoxia hypoxia-inducible factor ALPHA Hepatocellu
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褪黑素通过下调HIF-1α表达增强卵巢癌细胞OVCAR3顺铂敏感性
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作者 张海光 杨君 +3 位作者 郭会敏 张雪英 秦学娜 华方方 《现代肿瘤医学》 CAS 2024年第10期1804-1809,共6页
目的:探讨褪黑素对卵巢癌细胞顺铂敏感性的影响及其机制。方法:采用不同浓度褪黑素联合顺铂作用于卵巢癌细胞OVCAR3,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blot检测凋亡相关蛋白及信号通路蛋白AKT及ERK的磷酸化,同时检测... 目的:探讨褪黑素对卵巢癌细胞顺铂敏感性的影响及其机制。方法:采用不同浓度褪黑素联合顺铂作用于卵巢癌细胞OVCAR3,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blot检测凋亡相关蛋白及信号通路蛋白AKT及ERK的磷酸化,同时检测褪黑素对HIF-1α蛋白表达的影响。结果:MTT结果显示,褪黑素和顺铂联合作用能够显著抑制OVCAR3细胞增殖(P<0.05)。流式细胞仪检测结果显示,褪黑素和顺铂联合作用相较于单独顺铂作用或褪黑素作用能够显著增加OVCAR3细胞的凋亡。Western blot结果显示,褪黑素与顺铂联合作用能够增加促凋亡蛋白BAX及Caspase3的表达,抑制抗凋亡蛋白BCL2的表达,检测信号通路结果显示,褪黑素与顺铂联合作用能够促进AKT及ERK的磷酸化,同时褪黑素能够抑制HIF-1α蛋白的表达。结论:褪黑素通过抑制HIF-1α的表达使OVCAR3细胞对顺铂敏感。 展开更多
关键词 卵巢癌 褪黑素 顺铂 缺氧诱导因子1ɑ 凋亡相关蛋白
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吲哚-3-甲醇通过抑制mTOR/HIF-1α信号通路减弱低氧诱导的肺动脉平滑肌细胞增殖
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作者 陈昌贵 易春峰 +3 位作者 余志华 张帆 李佐民 贺立群 《中南药学》 CAS 2024年第9期2300-2306,共7页
目的观察吲哚-3-甲醇(I3C)对低氧诱导的肺动脉平滑肌细胞(PASMCs)增殖的作用。方法采用0.2%Ⅰ型胶原酶消化分离SD大鼠PASMCs,以低氧(1%O2)作为诱导剂,建立PASMCs增殖的细胞模型,以不同浓度的I3C(25、50、100、200μmol·L^(-1))干预... 目的观察吲哚-3-甲醇(I3C)对低氧诱导的肺动脉平滑肌细胞(PASMCs)增殖的作用。方法采用0.2%Ⅰ型胶原酶消化分离SD大鼠PASMCs,以低氧(1%O2)作为诱导剂,建立PASMCs增殖的细胞模型,以不同浓度的I3C(25、50、100、200μmol·L^(-1))干预24 h,检测细胞增殖及存活率;设置哺乳动物雷帕霉素靶蛋白(mTOR)抑制剂rapamycin或缺氧诱导因子-1α(HIF-1α)抑制剂LW6为阳性对照组,以100μmol·L^(-1 )I3C,HIF-1α稳定剂DMOG或mTOR激活剂MHY1485干预24 h后,CCK-8试剂盒检测细胞增殖;流式细胞仪检测细胞周期;Western blot检测HIF-1α、总的mTOR及磷酸化的mTOR和细胞周期调控相关蛋白的表达,确定I3C抑制PASMCs增殖的作用机制。结果25~100μmol·L^(-1 )I3C抑制低氧诱导的PASMCs增殖的作用具有浓度依赖性(P<0.05),而100μmol·L^(-1)与200μmol·L^(-1 )I3C抑制细胞增殖的作用无明显差异,且I3C无明显细胞毒性作用。I3C(100μmol·L^(-1))与LW6均可抑制低氧诱导的PASMCs增殖,阻滞细胞周期于G0/G1期,抑制HIF-1α、细胞周期蛋白(Cyclin)D1、Cyclin E、细胞周期蛋白依赖性激酶(CDK)2、CDK4和CDK6的表达(P<0.05),且DMOG能够逆转I3C的上述作用(P<0.05)。另外I3C与rapamycin在抑制低氧诱导的PASMCs增殖与mTOR/HIF-1α信号通路活化方面作用相似,且MHY1485能够逆转I3C抑制细胞增殖及mTOR/HIF-1α信号通路活化的作用(P<0.05)。结论I3C可通过抑制mTOR/HIF-1α信号通路减弱低氧诱导的PASMCs增殖。 展开更多
关键词 低氧 肺动脉平滑肌细胞 吲哚-3-甲醇 增殖 哺乳动物雷帕霉素靶蛋白/缺氧诱导因子1α
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Antisense Oligonucleotide of Hypoxia-inducible Factor-1alpha Suppresses Growth and Tumorigenicity of Lung Cancer Cells A549 被引量:2
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作者 张万广 张惠兰 邢丽华 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2006年第4期448-450,共3页
Summary: To study the role and mechanisms of hypoxia-inducible factor-lalpha (HIF-1α on the growth and tumorigenicity of lung cancer cells A549, the antisense oligonucleotide of HIF-1α was transfected to A549 cell... Summary: To study the role and mechanisms of hypoxia-inducible factor-lalpha (HIF-1α on the growth and tumorigenicity of lung cancer cells A549, the antisense oligonucleotide of HIF-1α was transfected to A549 cells. The effect of the antisense oligonucleotide on tumor growth in vitro and in vivo was evaluated by the growth rate suppression of A549 cells and subcutaneous implanted tumor in nude mice, and the effect on tumorigenicity was evaluated by the expression inhibition of angiogenic factors, the microvessel density (MVD)and vascular endothelial growth factor (VEGF) protein expression which were detected by immohistochemistry and western blot respectively. This study revealed that in vitro the growth rate of antisense oligonucleotide group was significantly decreased as compared with that of control group, sense oligonucleotide group and false-sense oligonucleotide group; in vivo the weight of implanted tumors in nude mice of antisense oligonucleotide group was 1.51±0.40 g, which was significantly lower than that of control group (2.79±0.33 g), sense oligonucleotide group (2.81±0.45g) and false-sense oligonucleotide group (2.89±0.39 g) and the inhibitory rate was 47 %. Both MVD and VEGF protein expression were significantly inhibited in antisense oligonucleotide group compared with those in other groups. These results indicated that antisense oligonucleotide of HIF-1α could inhibit lung cancer cells A549 growth in vitro and in vivo, and the mechanism may be due to the inhibition of vascular growth and VEGF protein expression. 展开更多
关键词 hypoxia inducible factor-lalpha antisense oligonucleotide vascular endothelial growth factor
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Expression of caspase-3 and hypoxia inducible factor 1αin hepatocellular carcinoma complicated by hemorrhage and necrosis 被引量:3
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作者 Hui Liang Jian-Guo Wu +4 位作者 Fei Wang Bo-Xuan Chen Shi-Tian Zou Cong Wang Shuai-Wu Luo 《World Journal of Clinical Cases》 SCIE 2021年第23期6725-6733,共9页
BACKGROUND Hepatocellular carcinoma(HCC)is a malignant tumor that occurs in the liver.Its onset is latent,and it shows high heterogeneity and can readily experience intrahepatic metastasis or systemic metastasis,which... BACKGROUND Hepatocellular carcinoma(HCC)is a malignant tumor that occurs in the liver.Its onset is latent,and it shows high heterogeneity and can readily experience intrahepatic metastasis or systemic metastasis,which seriously affects patients’quality of life.Numerous studies have shown that hypoxia inducible factor1α(HIF-1α)plays a significant role in the occurrence and development of tumors,as it promotes the formation of intratumoral vessels and plays a key role in their metastasis and invasion.Some studies have reported that caspase-3,which is induced by various factors,is involved in the apoptosis of tumor cells.AIM To investigate the expression of caspase-3 and HIF-1αand their relationship to the prognosis of patients with primary HCC complicated by pathological changes of hemorrhage and necrosis.METHODS A total of 88 patients with HCC complicated by pathological changes of hemorrhage and necrosis who were treated at our hospital from January 2017 to December 2019 were selected.The expression of caspase-3 and HIF-1αin HCC and paracancerous tissues from these patients was assessed.RESULTS The positive expression rate of caspase-3 in HCC tissues was 27.27%,which was significantly lower than that in the paracancerous tissues(P<0.05),while the positive expression rate of HIF-1αwas 72.73%,which was significantly higher than that in the paracancerous tissues(P<0.05).The positive expression rates for caspase-3 in tumor node metastasis(TNM)stage III and lymph node metastasis tissues were 2.78%and 2.50%,respectively,which were significantly lower than those in TNM stage I-II and non-lymph node metastasis tissues(P<0.05).The positive expression rates of HIF-1αin TNM stage III,lymph node metastasis,and portal vein tumor thrombus tissues were 86.11%,87.50%,and 88.00%,respectively,and these values were significantly higher than those in TNM stage I-II,non-lymph node metastasis,and portal vein tumor thrombus tissues(P<0.05).The expression of caspase-3 and HIF-1αin HCC tissues were negatively correlated(rs=−0.426,P<0.05).The median overall survival time of HCC patients was 18.90 mo(95%CI:17.20–19.91).The results of the Cox proportional risk regression model analysis showed that TNM stage,portal vein tumor thrombus,lymph node metastasis,caspase-3 expression,and HIF-1αexpression were the factors influencing patient prognosis(P<0.05).CONCLUSION The expression of caspase-3 decreases and HIF-1αincreases in HCC tissues complicated by pathological changes of hemorrhage and necrosis,and these are related to clinicopathological features and prognosis. 展开更多
关键词 Hepatocellular carcinoma CASPASE-3 hypoxia inducible factor HEMORRHAGE NECROSIS PROGNOSIS
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