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蛋白激酶C在肝细胞缺氧预处理中的作用 被引量:2
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作者 单毓强 高毅 +1 位作者 王瑜 潘明新 《世界华人消化杂志》 CAS 2003年第6期723-725,共3页
目的:研究蛋白激酶C(PKC)在肝细胞缺氧预处理中的作用, 方法:建立体外肝细胞缺氧预处理模型,应用PKC抑制剂白屈菜季铵碱(chelerythrine chloride,CHE)和激动剂豆蔻酸佛波酰乙酯(phorobol12-myristate13-acetate,PMA),通过检测PKC磷酸化... 目的:研究蛋白激酶C(PKC)在肝细胞缺氧预处理中的作用, 方法:建立体外肝细胞缺氧预处理模型,应用PKC抑制剂白屈菜季铵碱(chelerythrine chloride,CHE)和激动剂豆蔻酸佛波酰乙酯(phorobol12-myristate13-acetate,PMA),通过检测PKC磷酸化活性,细胞存活率,同时在透射电镜下观察肝细胞超微结构改变,研究PKC的作用,对相关数据进行统计学处理。结果:和缺氧复氧组的PKC磷酸化活性(710.5±78.8)fkat/g比较,缺氧预处理组的PKC磷酸化活性(1823.7±2682)fkat/g和PKC激动剂组的PKC磷酸化活性(2541.2±326.5)fkat/g显著增高(P<0.01),肝细胞结构损伤改变较小;和缺氧预处理组比较,PKC抑制剂组相应指标呈相反的变化,PKC磷酸化活性(1088.0±89.3)fkat/g(P<0.01)。结论:肝细胞缺氧预处理细胞保护作用中,PKC通路起到至关重要的作用。 展开更多
关键词 蛋白激酶C 肝细胞缺氧 预处理 细胞存活率 蛋白激酶C抑制剂 细胞保护
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大鼠肝细胞缺氧预处理后基因表达谱的改变 被引量:1
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作者 陈炜 吴志勇 +3 位作者 邱江峰 张志奇 罗海峰 Joan Rosello-Catafau 《中华外科杂志》 CAS CSCD 北大核心 2005年第21期1405-1406,共2页
关键词 缺氧预处理 大鼠细胞 基因表达谱 基因芯片技术 缺血预处理 再灌注损伤 肝细胞缺氧 离体培养 信号传导 受体介导
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^(131)I治疗甲亢肝损害的临床观察 被引量:4
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作者 王洪生 袁香坤 张立东 《放射免疫学杂志》 CAS 2007年第3期249-249,共1页
关键词 甲亢患者 ^131I治疗 损害 临床观察 细胞变性坏死 甲状腺激素 高代谢状态 肝细胞缺氧
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缺氧诱导因子-1α及其靶基因在人肝癌HepG2细胞中的表达和意义 被引量:5
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作者 杜静 赵秋 +4 位作者 谷华 滕晓丽 覃华 刘南植 梁扩寰 《中华肝脏病杂志》 CAS CSCD 北大核心 2006年第8期607-609,共3页
缺氧诱导因子-1(HIF-1)存在于大多数实体肿瘤中,是肿瘤细胞维持氧平衡的重要的转录调节子。HIF-1包含α和β两个亚基(HIF-1α和HIF-1β),其中HIF-1α是主要的功能亚基,对HIF-1的转录活性起关键作用。缺氧条件下,HIF-1α被运输... 缺氧诱导因子-1(HIF-1)存在于大多数实体肿瘤中,是肿瘤细胞维持氧平衡的重要的转录调节子。HIF-1包含α和β两个亚基(HIF-1α和HIF-1β),其中HIF-1α是主要的功能亚基,对HIF-1的转录活性起关键作用。缺氧条件下,HIF-1α被运输到核内,与HIF—1β形成二聚体,通过与靶基因上的缺氧反应元件(HRE)结合而促进靶基因转录,其蛋白质产物发挥多种生物学功能,如参与肿瘤血管的形成与发展,肿瘤细胞能量代谢,肿瘤细胞增殖与存活等。 展开更多
关键词 细胞 缺氧 缺氧诱导因子-1 血管内皮生长因子
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巨噬细胞移动抑制因子在重型乙型肝炎肝组织中的表达 被引量:1
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作者 于晓辉 张方信 +2 位作者 刘聪 钱震 赵连三 《中华传染病杂志》 CAS CSCD 北大核心 2007年第3期178-180,共3页
感染HBV可引起重型肝炎,由于其高发病率、高病死率及发病机制复杂,始终是医学研究的热点。其发病机制主要涉及机体免疫应答、内毒素与细胞因子的共同作用。Tc细胞在清除HBV的同时,不但损伤肝细胞,其免疫复合物还可激活补体系统,引... 感染HBV可引起重型肝炎,由于其高发病率、高病死率及发病机制复杂,始终是医学研究的热点。其发病机制主要涉及机体免疫应答、内毒素与细胞因子的共同作用。Tc细胞在清除HBV的同时,不但损伤肝细胞,其免疫复合物还可激活补体系统,引起肝细胞大片坏死,尤其是内毒素血症诱导单核-巨噬细胞产生大量TNF-α、IL-6和IL-1等,可引起肝细胞膜损伤、微循环障碍及弥散性血管内凝血(DIC),从而导致肝细胞缺氧、坏死。 展开更多
关键词 单核-巨噬细胞 重型乙型 移动抑制因子 组织 弥散性血管内凝血 肝细胞缺氧 内毒素血症 细胞膜损伤
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Isoflurane preserves energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation 被引量:4
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作者 QuanLi Wei-FengYu +5 位作者 Mai-TaoZhou XinLu Li-QunYang MingZhu Jian-GangSong Jun-HuaLu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第25期3920-3924,共5页
AIM: To investigate the protective effect of isoflurane on energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation, and to compare isoflurane with halothane. METHODS: Hepatocytes freshly isolated f... AIM: To investigate the protective effect of isoflurane on energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation, and to compare isoflurane with halothane. METHODS: Hepatocytes freshly isolated from fed rats were suspended in Krebs-Henseleit buffer, and incubated in sealed flasks under O2/CO2 or N2/CO2 (95%/5%, V/V) for 30 or 60 min, followed by 5 or 10 min of reoxygenation, with an added volatile anesthetic or not. ATP, ADP, and adenosine monophosphate in hepatocytes were determined by high performance liquid chromatography, and energy charge was calculated. RESULTS: During 30 min of anoxia, the energy charge and total adenine nudeotide steadily increased with the isoflurane dose from 0 to 2 minimum alveolar anesthetic concentration (MAC), then decreased from 2 to 3 MAC. In short incubations (30-35 min) at 1 MAC isoflurane, energy charge modestly decreased during anoxia, which was partially prevented by isoflurane and completely reversed by reoxygenation, and total adenine nudeotide did not decrease. In long incubations (60-70 min), both energy charge and total adenine nudeotide greatly decreased during anoxia, with partial and no reversal by reoxygenation, respectively. Isoflurane partly prevented decreases in both energy charge and total adenine nudeotide during anoxia and reoxygenation. In addition, 1 MAC isoflurane obviously increased ATP/ADP, which could not be changed by 1 MAC halothane. CONCLUSION: Isoflurane partially protects isolated hepatocytes against decreases in both energy charge and total adenine nudeotide during short (reversible) or long (irreversible) anoxia. 展开更多
关键词 ISOFLURANE HEPATOCYTES ANOXIA Energy balance
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Estradiol-17β protects against hypoxia-induced hepatocyte injury through ER-mediated upregulation of Bcl-2 as well as ER-independent antioxidant effects 被引量:4
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作者 Min Young Lee Sun Chul Jung +1 位作者 Jang Hem Lee Ho Jae Han 《Cell Research》 SCIE CAS CSCD 2008年第4期491-499,共9页
Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. Thi... Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17β (E2) (10^-8s M) on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [^3H]-thymidine incorporation, and these phenomena were prevented through treatment with E2. Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E2 induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E2 on Bcl-2 and caspase expression were blocked by ICI 182780 (E2 receptor (ER) antagonist, 10"7 M). In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species (ROS) generated. These effects were blocked by E2, but not by E2-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase (MAPK), c-JUN N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and nuclear factor-kB (NF-kB). These effects were blocked by E2, but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kB activation. In conclusion, E2 was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/ SAPK and NF-kB. 展开更多
关键词 HYPOXIA estradiol-17β chicken hepatocytes
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Polycomb chromobox 4 enhances migration and pulmonary metastasis of hepatocellular carcinoma cell line MHCC97L 被引量:10
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作者 MEI Zhu JIAO HuiKe +3 位作者 WANG Wei LI Jie CHEN GuoQiang XU Ying 《Science China(Life Sciences)》 SCIE CAS 2014年第6期610-617,共8页
We recently report that the expression of polycomb chromobox 4(Cbx4)is significantly correlated with the overall survival of a great cohort of hepatocellular carcinoma(HCC)patients and it enhances hypoxia-induced vasc... We recently report that the expression of polycomb chromobox 4(Cbx4)is significantly correlated with the overall survival of a great cohort of hepatocellular carcinoma(HCC)patients and it enhances hypoxia-induced vascular endothelial growth factor(VEGF)expression and angiogenesis in HCC cells through enhancing sumoylation of hypoxia inducible factor-1alpha(HIF-1α).Here we continue to investigate the potential effects of Cbx4 on the migration and metastasis of the metastatic HCC cell line MHCC97L.Our results show that Cbx4 overexpression in the cell line increases the in vitro vessel formation of vascular endothelial cells in its SUMO interaction motifs-dependent manner,and promotes the in vitro migration of the cancer cell,which can be effectively abrogated by anti-VEGF antibody.Although Cbx4 expression does not impact the in vitro growth of MHCC97L cells,it still promotes the progression and metastasis of orthotopically transplanted tumors in nude mice.These results further support the role of Cbx4 as a SUMO E3 ligase in the progression and metastasis of HCC. 展开更多
关键词 polycomb chromobox 4 hepatocellular carcinoma vascular endothelial growth factor METASTASIS
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