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国家自然科学基金(81100485)

作品数:4 被引量:14H指数:2
相关作者:王迪葛树旺徐钢韩敏郭水明更多>>
相关机构:华中科技大学更多>>
发文基金:国家自然科学基金教育部留学回国人员科研启动基金更多>>
相关领域:医药卫生更多>>

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IgA肾病合并抗肾小球基底膜病病例报告并文献复习被引量:6
2015年
目的:探讨IgA肾病合并抗肾小球基底膜(GBM)病的临床表现、诊断、治疗及预后。方法:回顾性分析我院1例IgA肾病合并抗GBM病患者的临床资料,并对相关文献进行复习。结果:以肉眼血尿和进行性升高血肌酐为主要表现,既往肾活检示IgA肾病,此次入院查抗GBM阳性,考虑IgA合并抗GBM病,给予激素免疫抑制剂冲击治疗、血浆置换、规律透析治疗,但是肾功能无明显恢复。结论:IgA肾病和抗GBM病均是免疫复合物相关性疾病,两者可同时出现,及早发现、及早诊治,可有助于挽救患者的肾脏功能。
尚伟锋王迪葛树旺郭水明徐钢韩敏
关键词:IGA肾病
Downregulation of p38 MAPK Involved in Inhibition of LDL-induced Proliferation of Mesangial Cells and Matrix by Curcumin被引量:1
2013年
Curcumin, as a main pharmacological component in the traditional Chinese medicine-- tttrmeric, has shown anti-inflammatory, anti-oxidation, anti-tumor and anti-fibrotic effects. This study aimed to investigate the possible underlying signaling pathway which was involved in the inhibition of LDL-induced proliferation of mesangial cells and matrix by curcumin. Rat mesangial cells in vitro were incubated with low-density lipoprotein (LDL) and different concentrations of curcumin (0, 6.25, 12.5, 25.0 9mol/L) or p38 MAPK inhibitor, SB203580 (10 μmol/L). Under LDL incubation, mesangial cells proliferated, the expression of MMP-2 mRNA and protein was decreased, the expression of COX-2 mRNA and protein was increased, reactive oxygen species (ROS) generation was increased and p38 MAPK was activated significantly (P〈0.05). When LDL-induced cells were treated with curcumin in the concentration of 12.5 or 25.0 μmol/L, LDL-induced proliferation ofmesangial cells was suppressed, the expression of MMP-2 mRNA and protein increased, the expression of COX-2 mRNA and protein downregulated, the production of ROS inhibited and p38 MAPK inactivated (P〈0.05). In conclusion, curcumin can inhibit the LDL-induced proliferation of mesangial cells and up-regulate the expression of MMP-2, which may be related with the inhibitory effect of curcumin on COX-2 expression, ROS pro- duction and p38 MAPK.
夏菊梅张俊周文祥刘晓城韩敏
关键词:CURCUMINCYCLOOXYGENASE-2
Erbin Interacts with Sema4C and Inhibits Sema4C-induced Epithelial-mesenchymal Transition in HK2 Cells被引量:1
2013年
Erbin, a member of Leucine-rich repeat and PDZ-containing protein family, was found to inhibit TGF-β-induced epithelial-mesenchymal transition (EMT) in our previous study. However, the mechanism of Erbin in regulating EMT is unclear. Semaphorin protein Sema4C, with PDZ binding site at C-terminal has been recognized as a positive regulator of EMT. Here, we aimed to examine the inter- action between Erbin and Sema4C. HK2 cells were treated with TGF-β1, or transfected with Erbin and (or) Sema4C. Interaction of Erbin and Sema4C was identified by immunoprecipitation. RT-PCR was used to detect the expression of Erbin and Sema4C at mRNA level after transfection. The expression levels of Erbin, Sema4C, and markers of EMT were measured by using Western blotting or ELISA. Af- ter HK2 cells were stimulated with 10 ng/mL TGF-β1 for 72 h, the protein expression levels of Erbin and Sema4C were both up-regulated, and immunoprecipitation results showed Erbin interacted with Sema4C in HK2 cells both at endogenous and exogenous levels. Furthermore, overexpression of Sema4C suppressed E-cadherin, induced vimentin and promoted fibronectin secretion, indicating Sema4C promotes the process of EMT. However, HK2 cells overexpressing Erbin were resistant to Sema4C-induced EMT. In contrast, Erbin specific siRNA promoted EMT induced by Sema4C. Taken together, these results suggest that Erbin can interact with Sema4C, and co-expression of Erbin blocks the process of Sema4C-induced EMT.
周巧丹宁勇曾锐陈琳寇沛许楚瓯裴广畅韩敏徐钢
关键词:ERBIN
Glucocorticoid Receptor Agonist Dexamethasone Attenuates Renal Ischemia/Reperfusion Injury by Up-regulating eNOS/iNOS被引量:6
2014年
The aim of this study was to determine the effect of dexamethasone(DEX) on renal ischemia/reperfusion injury(IRI). C57BL/6 mice were randomly divided into Sham group, IRI group and DEX group. The mice in IRI and DEX groups subjected to renal ischemia for 60 min, were treated with saline or DEX(4 mg/kg, i.p.) 60 min prior to I/R. After 24 h of reperfusion, the renal function, renal pathological changes, activation of extracellular signal-regulated kinase(ERK) and glucocorticoid receptor(GR), and the levels of iNOS and eNOS were detected. The results showed DEX significantly decreased the damage to renal function and pathological changes after renal IRI. Pre-treatment with DEX reduced ERK activation and down-regulated the level of iNOS, whereas up-regulated the level of eNOS after renal IRI. DEX could further promote the activation of GR. These findings indicated GR activation confers preconditioning-like protection against acute IRI partially by up-regulating the ratio of eNOS/iNOS.
张炯李俊华王艻韩敏肖芳兰小勤李月强徐钢姚颖
关键词:DEXAMETHASONE
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