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| 1 | 早期反应基因-1(Egr-1)在缺血再灌注肝脏组织中的表达显示文摘目的研究缺血再灌注后肝组织中早期反应基因-1(Egr-1)的表达。方法动脉放血至平均动脉压(MAP)25 mmHg,分别维持1 h或2.5 h,复制小鼠整体肝缺血模型;2.5 h后,回输失血+2倍于失血量的平衡液至MAP 80 mmHg,复制小鼠肝缺血再灌注模型。取肝组织,分别通过Northern印迹法、凝胶电泳迁移分析(EMSA)、蛋白质免疫印迹法,检测肝组织mRNA的表达;肝核提取物中Egr-1蛋白与DNA的结合活性;肝组织、胞浆及核提取物中Egr-1蛋白的表达。结果缺血1 h后,Egr-1mRNA在肝组织中的表达明显增强;缺血2.5 h后肝组织中Egr-1mRNA虽有所下降,但表达水平仍较高。缺血2.5 h+再灌注4 h后,肝组织中Egr-1mRNA消失。缺血2.5 h和缺血2.5 h+再灌注4 h后肝细胞核提取物中Egr-1蛋白的DNA结合活性增加。缺血2.5 h及缺血2.5 h+再灌注4 h肝组织及肝细胞核提取物中Egr-1蛋白表达明显增加;Egr-1蛋白仅在缺血2.5 h肝胞浆提取物中表达。结论本实验结果表明肝缺血再灌注后Egr-1mRNA和蛋白表达均明显增强,其DNA结合活性增加,说明其转录和翻译水平均增加。本研究显示缺血再灌注后肝脏中Egr-1基因被激活,Egr-1可能参与了肝I/R后炎症反应基因的调节,并在肝损伤中起一定的作用。 | 梅建民 Ti mothy R.Billiar 吕民生 David J.Gallo 杨荣华 聂洪峰 | 2005 | 中华肝胆外科杂志2005，11，11： | 3 |
| 2 | 氨甲蝶呤抑制小鼠巨噬细胞一氧化氮合酶表达显示文摘研究氨甲蝶呤 (MTX)在小鼠巨噬细胞 (RAW2 6 4 7)对一氧化氮合酶 (NOS)表达的抑制作用。本试验应用内毒素 (LPS)、干扰素 (IFNr)、MTX、二氨基 羟基嘧啶 (DAHP) ,四氢生物喋呤 (BH4 )刺激 8h后 ,用Northern杂交检测NOSmRNA水平和GTP CH 1mRNA水平表达 ,并用Griessreaction方法检测NO2- NO3- 浓度 ,用Duch方法测定GTP CH 1活性值。我们发现 ,MTX在小鼠巨噬细胞 (RAW2 6 4 7)对NOSmRNA水平和GTP CH 1mRNA水平表达有轻度抑制作用 ,对NO2- NO3- 浓度和GTP CH 1活性抑制作用较弱。MTX和DAHP联合应用不仅对NOSmRNA水平和GTP CH 1mRNA水平表达抑制作用较强 ,而且对NO2- NO3 浓度和GTP CH 1活性抑制较大。BH4的加入可以减少MTX和DAHP对一氧化氮 (NO)生成的抑制作用。 | 刘质泽 Timothy R.Billiar | 2002 | 基础医学与临床2002，22，3： | 2 |
| 3 | Expression of Egr-1 in the liver of mice following hemorrhagic shock and resuscitation显示文摘Objective: To investigate the expression of early growth response gene-1(Egr-1) in the liver following hemorrhagic shock with or without resuscitation(HS or HSR). Methods: Mice were subjected to HS or HSR.Liver expression of Egr-1 mRNA was detected by Northern blotting.DNA binding activity of the Egr-1 protein in liver nuclear extracts(NE) was determined by electrophoretic mobility shift assay(EMSA).Western blot analysis was used to assess the induction of Egr-1 protein in the liver tissue,cytoplasma and NE. Results: Egr-1 mRNA was strongly expressed as early as 1 h after HS,and its level was decreased in the following 2.5 h but still higher than that in 1 h HS group.The Egr-1 DNA binding activity elevated in the liver NE of 2.5 h HS group and 2.5 h HS + 4 h R group,so did the Egr-1 protein in the liver and the liver NE of the same two groups.However,the maximal Egr-1 protein expression was found in the cytoplasma of liver following 2.5 h HS. Conclusion: Our data suggest that both Egr-1 mRNA and protein are strongly elevated and the binding activity of Egr-1 to its cognate DNA site is increased in the liver following HSR,indicating the increases of Egr-1 transcriptional and translational levels.This study provides evidence that Egr-1 gene is activated in the liver during HS and HSR. | 梅建民 Timothy R.Billiar 于聪慧 David J.Gallo 杨荣华 | 2005 | Journal of Medical Colleges of PLA(China)2005，20，2： | 1 |
| 4 | 转录因子Egr-1在失血性休克复苏后肝脏损伤中的作用显示文摘目的研究转录因子 Egr-1在失血性休克复苏(HS/R)后肝脏损伤中的作用。方法利用 Egr-1野生型(WT)和基因封闭型(KO)小鼠复制失血性休克复苏模型。取肝组织,RT-PCR 法测定肝组织中 TNF-α、IL-6、G-CSF、ICAM-1 mRNA 的表达变化。通过检测肝组织中 MPO 的含量、血清 ALT 水平和组织学检查,评估肝脏炎症细胞浸润和损伤程度。结果失血性休克2.5 h+复苏4h 后,Egr-1 KO 小鼠肝组织中 TNF-α、IL-6、G-CSF、ICAM-1 mRNA 的表达水平明显低于Egr-1WT 组;Egr-1 KO 组失血性休克复苏后肝组织炎性浸润和损伤程度减轻,表现为血清 ALT 水平低,肝组织中 MPO 含量低,病理损伤轻。结论本实验结果表明转录因子 Egr-1参与了失血性休克复苏后肝脏炎症反应基因表达的调节,在失血性休克复苏后的肝脏损伤中起一定的作用。 | 梅建民 Timothy R.Billiar 于聪慧 David J.Gallo 杨荣华 刘沙雷 | 2006 | 中华肝胆外科杂志2006，12，5： | 1 |
| 5 | Hydrogen Inhalation Ameliorates Oxidative Stress in Transplantation Induced Intestinal Graft Injury显示文摘 | B. M.Buchholz D. J.Kaczorowski R.Sugimoto R.Yang Y.Wang T. R.Billiar K. R.McCurry A. J.Bauer A.Nakao | 2008 | American Journal of Transplantation2008，，10： | 1 |
| 6 | Role of transcription factor Egr-1 in liver injury following hemorrhagic shock and resuscitation显示文摘Objective: To investigate the role of transcription factor Egr-1 in liver injury following hemorrhagic shock (HS) /resuscitation (R). Methods: Both Egr-1 knockout (KO) and wild-type (WT) mice were subjected to HS and HSR injuries. The expressions of TNF-α, IL-6, G-CSF and ICAM-1 mRNAs in the liver were examined by RT-PCR, and their serum levels were measured by ELISA. The liver inflammatory infiltration and liver injury in both Egr-1 WT and KO mice following HS/R were evaluated by liver MPO content, serum ALT level and histological examination. Results: Egr-1 inhibition resulted in less mRNA expression of TNF-α, IL-6 , G-CSF and ICAM-1 in the liver, and lower serum levels of TNF-α, IL-6, G-CSF and ICAM-1 antigens in Egr-1 KO mice following HS/R. The liver inflammatory infiltration and liver injury were less severe in Egr-1 KO mice following HS/R, as evidenced by lower serum ALT level, lower hepatic MPO content and histological manifestations. Conclusion: Our data suggest that transcription factor Egr-1 is involved in regulating the expression of inflammatory response genes and plays a role in liver injury following HS/R. | 梅建民 Timothy R.Billiar 于聪慧 David J.Gallo 杨荣华 刘沙雷 | 2005 | Journal of Medical Colleges of PLA(China)2005，20，2： | 0 |
| 7 | Correction to:EGFR signaling augments TLR4 cell surface expression and function in macrophages via regulation of Rab5a activation显示文摘Figure 1.EGFR activation promotes TLR4 phosphorylation and cell surface expression of TLR4 in response to LPS.(A and B)BMDM were treated with LPS(1μg/mL)for 6,12,or 24 h in the presence or absence of pretreatment of PD or TAPI-1.(A)Flow cytometry analysis of cell surface TLR4 intensity in BMDM.(B)Flow cytometry analysis of cell surface TLR4 intensity in BMDM.(C and D)WT(C57BL76)mice were treated with LPS(10 mg/kg,i.p.).In some groups,mice were pretreated with erlotinib(100 mg/kg,gavage administration)at 30 min prior to LPS i.p. | Jing Tang Bowei Zhou Melanie J.Scott Linsong Chen Dengming Lai Erica K.Fan Yuehua Li Qiang Wu Timothy R.Billiar Mark A.Wilson Ping Wang Jie Fan | 2020 | Protein & Cell2020，11，8： | 0 |
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