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| 1 | 非酒精性脂肪性肝病中脂毒性肝细胞来源的外泌体miR-192-5p通过Rictor/Akt/FoxO1信号通路激活巨噬细胞显示文摘【据Hepatology 2020年5月报道】题:非酒精性脂肪性肝病中脂毒性肝细胞来源的外泌体miR-192-5p通过Rictor/Akt/FoxO1信号通路激活巨噬细胞(作者Liu XL等)肝脏巨噬细胞可被多种因素如肠道菌群代谢物以及受损的肝细胞释放物等激活。在非酒精性脂肪性肝病(NAFLD)的发生发展中,巨噬细胞向促炎表型(M1)的极化是一个重要的病理生理过程。外泌体可传递多种生物学成分如microRNA、蛋白质以及脂质等,因此被作为细胞间通讯的重要媒介。在NAFLD的发生发展过程中,外泌体在肝细胞与巨噬细胞对话中的作用尚未明确。 | 刘晓琳 范建高 LIU XL PAN Q CAO HX | 2020 | 临床肝胆病杂志2020，36，10： | 28 |
| 2 | A metabonomic investigation on the biochemical perturbation in liver failure patients caused by hepatitis b virus显示文摘 | Yu, K Sheng, GP Sheng, JF Chen, YM Xu, W Liu, XL Cao, HC Qu, HB Cheng, YY Li, LJ | 2007 | 中国生物学文摘2007，21，11： | 25 |
| 3 | Upregulation of vimentin and aberrant expression of E-cadherin /beta-catenin complex in oral squamous cell carcinomas:correlation with the clinicopathological features and patient outcome显示文摘Oral squamous cell carcinoma is a challenging oncology problem.A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined.Using quantitative immunohistochemistry,we examined the expression of vimentin,E-cadherin,and beta-catenin in 83 oral squamous cell carcinoma patients,and the relationships between the expression of these markers and specific clinicopathological features were analysed.The high expression of vimentin was observed in 23 of 43(53%) tumours from patients who eventually developed a recurrent tumour and was associated with recurrence and death(P < 0.001 and < 0.001,respectively).The decreased expression of E-cadherin was observed in 36 of 43(84%) tumours from patients who eventually developed a recurrent tumour and was also associated with recurrence and death(P < 0.001 and < 0.001,respectively).Although no correlation between beta-catenin expression in whole-tumour sections and clinicopathological features was observed,decreased beta-catenin expression at the tumour invasive front was closely associated with recurrence and death(P=0.002 and 0.002,respectively).The expression of vimentin and that of E-cadherin were associated with survival and were independent prognostic factors in univariate and multivariate analyses.Our data show that the overexpression of vimentin was closely associated with recurrence and death in oral squamous cell carcinoma patients.The combination of the upregulation of vimentin and aberrant expression of E-cadherin/beta-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma. | Liu,LK Jiang,XY Zhou,XX Wang,DM Song,XL Jiang,HB Nanjing Med Univ,Coll Stomatol,Dept Oral Pathol,Nanjing 210029,Jiangsu,Peoples R China Nanjing Med Univ,Inst Stomatol,Dept Oral Pathol,Nanjing 210029,Jiangsu,Peoples R China Nanjing Med Univ,Coll Stomatol,Dept Oral & Maxillofacial Surg,Nanjing 210029,Jiangsu,Peoples R China | 2010 | 南京医科大学学报(自然科学版)2010，30，5： | 25 |
| 4 | Effects of salvianolic acid-A on NIH/3T3 fibroblast proliferation,collagen synthesis and gene expression显示文摘AIM To investigate the mechanisms ofsalvianolic acid A(SA-A)against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10-4mol/L-10-7mol/L SA-A for 22 h.The cell viability wasassayed by[3H]proline incorporation,cellproliferation by[3H]TdR incorporation,cellcollagen synthetic rate was measured with[3H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α(1)I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10-4mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10-5mol/L-10-7mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10-6mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10-5mol/L-10-6mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10-5mol/L and10-6mol/L SA-A could decrease α(1)I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug. | Liu CH Hu YY Wang XL Liu P Xu LM | 2000 | World Journal of Gastroenterology2000，6，3： | 25 |
| 5 | Association of N-terminal pro-brain natriuretic peptide with the severity of coronary artery disease in patients with normal left ventricular ejection fraction显示文摘 | Wu NQ Guo YL Li XL Liu J Qing P Xu RX Zhu CG Jia Y J Liu G Dong Q Jiang LX Li J J Ma FL | 2014 | Chinese Medical Journal2014，，4： | 23 |
| 6 | Down-regulation of Hsp90 could change cell cycle distribution and increase drug sensitivity of tumor cells显示文摘:AIM To construct Hsp90 antisense RNAeukaryotic expression vector, transfect it intoSGC7901 and SGC7901/VCR of MDR-type humangastric cancer cell lines, HCC7402 of humanhepatic cancer and Eel09 of human esophagealcancer cell lines, and to study the cell cycledistribution of the gene transected cells andtheir response to chemotherapeutic drugs.METHODS A I .03kb cDNA sequence of Hsp90Pwas obtained from the primary plasmid phHsp90by EcoR 1 and BamH I nuclease digestion andwas cloned to the EcoR 1 and BamH 1 site ofthe pcDNA by T4DNA ligase and an antisenseorientation of Hsp900 expression vector wasconstructed. The constructs were transfectedwith lipofectamine and positive clones wereselected with G418. The expression of RNA wasdetermined with dot blotting and RNaseprotection assay, and the expression of Hsp90protein determined with Western blot. Cell cycledistribution of the transfectants was analyzedwith flow cytometry, and the drug sensitivity ofthe transfectants to adriamycin (ADR ),vincrinstine (VCR ), mitomycin (MMC ) andcyclophosphamide (CTX ) with MTT andintracellular drug concentration of thetransfectants was determined with flowcytometry.RESULTS In EcoR 1 and BamH I restrictionanalysis, the size and the direction of the clonedsequence of Hsp900 remained what had beendesigned and the gene constructs were namedpcDNA-Hsp90. AH^SGC7901, AH^SGC7901/ VCR,AH-HCC7402 and AH-Eel09 cell clones allexpressed Hsp90 anti--sense RNA. Theexpression of Hsp90 was down--regulated in AHSGC7901, AH--SGC7901/ VCR, AH-HCC7402 andAH--Eel09 cell clones. Cell cycle distribution waschanged differently. In AH-SGC7901/ VCR andAH-Ec109 cells, G, phase cells were increased; Sphase and G, phase cells were decreased ascompared with their parental cell lines. In AHSGC7901 cell, G, phase cells were decreased, Qphase cells increased and S phase cells were notchanged, and in AH-HCC7402 cells G,, S and qphase cells remained unchanged as comparedwith their parental cell lines. The sensitivity ofAH--SGC7901, AH--SGC7901/ VCR, AH-HCC7402 andAH-Ec109 to chemotherapeutic drugs, thesensitivity ot AH--SGC7901/ VCR to ADR, VCR,MMC and CTX the sensitivity of AH-HCC7402 toADR and VCR, and the sensitivity of Eel09 toADR, VCR and CTX all increased as comparedwith their parental cell lines. The meanfluorescence intensity of ADR in AH--SGC7901,AH-SGC7901/ VCR, AH--HCC7402 and AH-Ec109was also significantly elevated (P< 0. 05).CONCLUSION Down-regulation of HsP90 couldchange cell cycle distribution and increase thedrug sensitivity of tumor cells. | Liu XL Xiao B Yu ZC Guo JC Zhao QC Xu L Shi YQ Fan DM | 1999 | World Journal of Gastroenterology1999，5，3： | 21 |
| 7 | Protective effects of prostaglandin E1 on hepatocytes显示文摘INTRODUCTION E Numerous studies have demonstrated the protective action of prostaglandin E1(PGE1) on experimental animal models of liver injury and on patients with | Liu XL Fan DM | 2000 | World Journal of Gastroenterology2000，6，3： | 18 |
| 8 | The regulation of rotenone-induced inflammatory factor production by ATP-sensitive potassium channel expressed in BV-2 cells显示文摘 | Liu X Wu JY Zhou F Sun XL Yao HH Yang Y Ding JH Hu G | 2006 | 中国生物学文摘2006，20，10： | 11 |
| 9 | Byakangelicin induces cytochrome P450 3A4 expression via transactivation of pregnane X receptors in human hepatocytes显示文摘 | Yang, JA Luan, XF Gui, HY Yan, P Yang, DF Song, XL Liu, W Hu, G Yah, BF | 2011 | 南京医科大学学报(自然科学版)2011，31，4： | 8 |
| 10 | Estrogen provides neuroprotection against activated microglia-induced dopaminergic neuronal injury through both estrogen receptor-alpha and estrogen receptor-beta in microglia显示文摘 | Liu X Fan XL Zhao Y Luo GR Li XP Li R Le WD | 2006 | 中国生物学文摘2006，20，10： | 2 |
| 11 | MiR-126 restora-tion down-regulate VEGF and inhibit the growth of lung cancer celllines in vitro and in vivo显示文摘 | Liu B Peng XC Zheng XL Wang J Qin YW | 2009 | Lung Cancer2009，66，2： | 1 |
| 12 | West Nile Virus Infection in Xinjiang, China显示文摘 | Li XL Fu SH Liu WB | 2013 | Vector-Borne and Zoonotic Diseases2013，13，2： | 1 |
| 13 | Endothelial progenitor cells (EPCs) mobilized and activated by neurotrophic factors may contribute to pathologic neovascularization in diabetic retinopa-thy显示文摘 | Liu XL Li YJ Liu YZ | 2010 | Am J Pathol2010，176，1： | 1 |
| 14 | mmobilizing shortened single walled carbon nanotubes (SWNTs) on gold using a surface condensation method显示文摘 | Nan XL Gu ZN Liu ZF | 2002 | Journal of Colloid and Interface SeienceJ2002，245，2： | 1 |
| 15 | MiR-126 restora-tion down-regulate VEGF and inhibit the growth of lung cancer celllines in vitro and in vivo显示文摘 | Liu B Peng XC Zheng XL Wang J Qin YW | 2009 | Lung Cancer2009，66，2： | 1 |
| 16 | Remodelling of keloid tissue into normal-looking skin 显示文摘 | Liu W Wu XL Gao Z | 2008 | J Plast Reconstr Aesthet Surg2008，61，12： | 1 |
| 17 | MiR - 126 restorationdown - regulate VEGF and inhibit the growth of lung cancer celllines in vitro and in vivo显示文摘 | LIU B PENG X C ZHENG XL | 2009 | Lung Cancer2009，66，2： | 1 |
| 18 | Repair of extended peripheral nerve lesions in rhesus monkeys using acellular allogenic nerve grafts implanted with autologous mesenchymal stem cells显示文摘 | Hu J Zhu QT Liu XL | 2007 | Exp Neurol2007，204，： | 1 |
| 19 | A causal relationship between shear stress and atheroselerotic lesions in apolipoprotein E knockout mice assessed by ultrasound biomicroseopy显示文摘 | Ding SF Ni M Liu XL | | Am J Physiol Heart Circ Physiol0，298，： | 1 |
| 20 | MiR-126 restoration down-regulate VEGF and inhibit the growth of lung cancer cell lines in vitro and in vivo显示文摘 | Liu B Peng XC Zheng XL | 2009 | Lung Cancer2009，66，2： | 1 |
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