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A phosphatidylinositol 3-kinase/p70 ribosomal S6 protein kinase pathway is required for the regulation by insulin of the p85α regulatory subunit of phosphatidylinositol 3-kinase gene expression in human muscle cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 34005-34010页

作者： Roques, M Vidal, H Univ Lyon 1 Fac Med Rene Laennec INSERM U449 F-69372 Lyon 08 France

Insulin acutely up-regulates p85 alpha phosphatidylinositol 3-kinase (p85 alpha PI 3-K) mRNA levels in human skeletal muscle (Laville, M., Auboeuf, D., Khalfallah, Y., Vega, N., Riou, J, P., and Vidal, H. (1996) J. Clin. Invest. 98, 43-49), In the present work, we attempted to elucidate the mechanism of action of insulin in primary cultures of human muscle cells. Insulin (10(-7) M, 6 h of incubation) induced a a-fold increase in p85aPI3-K mRNA abundances (118 +/- 12 versus 233 +/- 35 amol/mu g total RNA, n = 5, p < 0.01) without changing the expression levels of insulin receptor, IRS-1, glycogen synthase, and Glut 4 mRNAs in differentiated myotubes from healthy subjects. The effect is most probably due to a transcriptional activation of the p85 alpha PI 3-K gene because the half-life of the mRNA was not affected by insulin treatment (4.0 +/- 0.8 versus 3.1 +/- 0.4 h), PD98059 (50 mu M) did not modify the insulin response but increased p85 alpha PI 3-K mRNA levels in the absence of insulin, suggesting that the mitogen-activated protein kinase pathway exerts a negative effect on p85 alpha PI 3-K mRNA expression in the absence of the hormone. On the other hand, the insulin effect was totally abolished by LY294002 (10 mu M) and rapamycin (50 nM). In addition, overexpression of a constitutively active protein kinase B increased p85 alpha PI 3-K mRNA levels. These results indicate that the phosphatidylinositol 3-kinase/PKB/p70S6 kinase pathway is required for the stimulation by insulin of p85 alpha PI 3-K gene expression in human muscle cells.

关键词：细胞培养的色酮类/药理学更生霉素/药理学剂量效应关系药物酶抑制剂/药理学类黄酮物质/药理学基因表达调控酶学/药物作用糖原合成酶/遗传学胰岛素/药理学胰岛素受体底物蛋白质类吗啉类/药理学肌骨骼/细胞学肌骨骼/药物作用肌骨骼/酶学磷酸肌醇3-激酶类/遗传学磷酸肌醇3-激酶类/代谢磷蛋白类/遗传学蛋白质合成抑制药/药理学蛋白质丝氨酸苏氨酸激酶原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学原癌基因蛋白质c-akt RNA 信使/药物作用 RNA 信使/遗传学 RNA 信使/代谢受体胰岛素/遗传学重组融合蛋白质类/遗传学重组融合蛋白质类/生理学调控序列核酸核糖体蛋白质S6激酶类/遗传学核糖体蛋白质S6激酶类/代谢信号传导西罗莫司/药理学转录遗传/药物作用成年人人类中年人

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Modulation of Ca²⁺/calmodulin-dependent protein kinase II activity by acute and chronic morphine administration in rat hippocampus:: Differential regulation of α and β isoforms

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MOLECULAR PHARMACOLOGY 1999年第3期55卷 557-563页

作者： Lou, LG Zhou, TH Wang, P Pei, G Chinese Acad Sci Shanghai Inst Cell Biol Shanghai 200031 Peoples R China

Calcium/calmodulin-dependent protein kinase II (CaMK II) has been shown to be involved in the regulation of opioid receptor signaling. The present study showed that acute morphine treatment significantly increased both Ca2+/calmodulin-independent and Ca2+/calmodulin-dependent activities of CaMK II in the rat hippocampus, with little alteration in the protein level of either alpha or beta isoform of CaMK II. However, chronic morphine treatment, by which rats were observed to develop apparent tolerance to morphine, significantly down-regulated both Ca2+/calmodulin-independent and Ca2+/calmodulin-dependent activities of CaMK II and differentially regulated the expression of a and beta isoforms of CaMK II at protein and mRNA levels. Application of naloxone or discontinuation of morphine treat-ment after chronic morphine administration, which induced the withdrawal syndrome of morphine, resulted in the overshoot of CaMK II (at both protein and mRNA levels) and its kinase activity. The phenomena of overshoot were mainly observed in the beta isoform of CaMK II but not in the a isoform. The effects of both acute and chronic morphine treatments on CaMK II could be completely abolished by the concomitant application of naloxone, indicating that the effects of morphine were achieved through activation of opioid receptors, Our data demonstrated that both acute and chronic morphine treatments could effectively modulate the activity and the expression of CaMK II in the hippocampus.

关键词：镇痛药阿片类/投药和剂量镇痛药阿片类/药理学基因表达/药物作用海马/药物作用海马/代谢吗啡/投药和剂量吗啡/药理学纳洛酮/药理学麻醉品拮抗药/药理学 RNA 信使/药物作用 RNA 信使/代谢大鼠 Sprague-Dawley 动物男(雄)性大鼠

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Ethanol and arachidonic acid increase α2(I) collagen expression in rat hepatic stellate cells overexpressing cytochrome P450 2E1 -: Role of H₂O₂ and cyclooxygenase-2

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第26期275卷 20136-20145页

作者： Nieto, N Greenwel, P Friedman, SL Zhang, F Dannenberg, AJ Cederbaum, AI Mt Sinai Sch Med Dept Biochem & Mol Biol New York NY 10029 USA Mt Sinai Sch Med Dept Med & Liver Dis New York NY 10029 USA Cornell Univ Weill Med Coll Dept Cardiothorac Surg New York NY 10021 USA Cornell Univ Weill Med Coll Dept Med New York NY 10021 USA Strang Canc Prevent Ctr New York NY 10021 USA

The ability of ethanol and arachidonic acid (AA), as inducers of oxidative stress and key factors in alcoholic liver disease, to up-regulate alpha 2 collagen type I (COL1A2) gene expression was studied in a hepatic stellate cell line overexpressing the ethanol-inducible cytochrome P450 2E1 (CYP2E1) (E5 cells). A time- and dose-dependent induction in COL1A2 mRNA by ethanol or AA was observed that was prevented by diallylsulfide, a CYP2E1 inhibitor, Nuclear run-on experiments showed transcriptional activation of the COL1A2 gene by ethanol and Ak Catalase abrogated the increase in COL1A2 mRNA suggesting an H2O2-dependent mechanism. Cyclooxygenase-2 (COX-2) levels and production of prostaglandin E-2 upon addition of AA were elevated in the E5 cells. Incubation with NS-398, a COX-2 inhibitor, blocked the effect of AA, but not of ethanol, on COL1A2 expression suggesting that CYP2E1 activates COX-2 expression, and the oxidation of AA by COX-2 is responsible for the increase in COL1A2. Activity of a reporter construct driven by -378 base pairs of the proximal promoter region of the COL1A2 gene increased in E5 but not control cells and was further increased by ethanol or AA. These experiments link CYP2E1-dependent oxidative stress to induction of COX-2 and the actions of ethanol and AA on activation of collagen gene expression in hepatic stellate cells.

关键词：烯丙化合物/药理学抗氧化剂/药理学花生四烯酸/药理学印迹法 RNA 印迹法蛋白质细胞系胶原/生物合成环氧化酶2 环氧化酶2抑制剂环加氧酶抑制药/药理学细胞色素P450CYP2E1/拮抗剂和抑制剂细胞色素P450CYP2E1/代谢剂量效应关系药物电泳聚丙烯酰氨凝胶乙醇/药理学基因报告过氧化氢/代谢同工酶类/代谢肝/药物作用模型生物学硝基苯甲酸盐/药理学氧化性应激前列腺素内过氧化物合酶类/代谢前列腺素E类/生物合成 RNA 信使/药物作用重组蛋白质类/代谢硫化物/药理学磺胺类/药理学时间因素转录遗传/药物作用动物大鼠

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Osteoprotegerin ligand modulates murine osteoclast survival in vitro and in vivo

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AMERICAN JOURNAL OF PATHOLOGY 2000年第2期157卷 435-448页

作者： Lacey, DL Tan, HL Lu, J Kaufman, S Van, G Qiu, WR Rattan, A Scully, S Fletcher, F Juan, T Kelley, M Burgess, TL Boyle, WJ Polverino, AJ Amgen Inc Dept Pharmacol Toxicol Thousand Oaks CA 91320 USA Amgen Inc Dept Cell Biol Thousand Oaks CA 91320 USA Amgen Inc Dept Mammalian Genom Thousand Oaks CA 91320 USA Amgen Inc Dept Prot Chem Thousand Oaks CA 91320 USA Amgen Inc Dept Mammalian Cell Mol Bio Thousand Oaks CA 91320 USA

Osteoprotegerin ligand (OPGL) targets osteoclast precursors and osteoclasts to enhance differentiation and activation, however, little is known about OPGL effects on osteoclast survival. In vitro, the combination of OPGL + colony-stimulating factor-1 (CSF-1) is required for optimal osteoclast survival. Ultrastructurally, apoptotic changes were observed in detached cells and culture lysates exhibited elevated caspase 3 activity, particularly in cultures lacking CSF-1, DEVD-FMK (caspase 3 inhibitor) partially protected cells when combined with OPGL, but not when used alone or in combination with CSF-1. CSF-1 maintained NF-kappa B activation and increased the expression of bcl-2 and bcl-X-L mRNA, but had no effect on JNK activation. In contrast, OPGL enhanced both NF-kappa B and JNK kinase activation and increased the expression of c-src, but not bcl-2 and bcl-X-L mRNA, These data suggest that aspects of both OPGL's and CSF-1's signaling/survival pathways are required for optimal osteoclast survival. In mice, a single dose of OPG, the OPGL decoy receptor, led to a >90% loss of osteoclasts because of apoptosis within 48 hours of exposure without impacting osteoclast precursor cells. Therefore, OPGL Is essential, but not sufficient, for osteoclast survival and endogenous CSF-1 levels are insufficient to maintain osteoclast viability in the absence of OPGL.

关键词：细胞凋亡/药物作用载体蛋白质类/药理学细胞存活/药物作用细胞培养的基因表达调控/药物作用糖蛋白类/药理学注射皮下巨噬细胞集落刺激因子/药理学膜糖蛋白类/药理学小鼠近交C3H NF-κB/代谢破骨细胞/细胞学破骨细胞/药物作用破骨细胞/超微结构骨保护素原癌基因蛋白质c-bcl-2/遗传学 RANK配体 RNA 信使/药物作用 RNA 信使/遗传学 RNA 信使/代谢核因子κB受体活化因子受体胞质和核受体肿瘤坏死因子时间因素 bcl-X蛋白质动物男(雄)性小鼠

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Differential expression of the rat γ-glutamyl transpeptidase gene promoters along with differentiation of hepatoblasts into biliary or hepatocytic lineage

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AMERICAN JOURNAL OF PATHOLOGY 2000年第2期157卷 537-548页

作者： Holic, N Suzuki, T Corlu, A Couchie, D Chobert, MN Guguen-Guillouzo, C Laperche, Y Univ Paris 12 Hop Henri Mondor INSERM U99 F-94010 Creteil France Hop Pontchaillou INSERM U522 Rennes France

gamma-Glutamyl transpeptidase (GGT), a major enzyme of glutathione (GSH) homeostasis, is often used as a biliary marker to follow the differentiation of hepatic precursor cells. The expression of the GGT gene is driven by different promoters and yields multiple mRNAs, depending on the cell type or the stage of differentiation. In the present study, we analyzed the GGT mRNA expression pattern by quantitative reverse transcriptase-polymerase chain reaction or by in situ hybridization i) in the liver, in vivo, at early stages of development;ii) in oval cells, which proliferate and differentiate into hepatocytes in response to galactosamine injury in vivo;and finally, iii) during hepatoblast differentiation, in vitro. We show that GGT gene transcription originates from promoters P3, P4, and P5 in rat hepatic precursor cells. Differentiation of these cells induces profound alterations in GGT gene expression, leading to extinction of promoters P4 and P5, when they differentiate into the hepatocytic pathway, and to extinction of promoters P3 and P5 when they differentiate into the biliary pathway. This diversity in GGT mRNA expression provides unique molecular probes to follow hepatic precursor cell differentiation. Furthermore, the identification of factors governing GGT P5 and P4 promoter expression should provide further insight into the molecular events that occur as the liver precursor cell differentiates into the hepatic lineages.

关键词：动物新生胆管/细胞学胆管/胚胎学胆管/酶学细胞分化细胞谱系细胞培养的半乳糖胺/药理学基因表达调控发育期/药物作用基因表达调控酶学/药物作用原位杂交肝/细胞学肝/胚胎学肝/酶学启动区遗传 RNA 信使/药物作用 RNA 信使/遗传学 RNA 信使/代谢大鼠 Wistar 逆转录聚合酶链反应 γ-谷氨酰转移酶/遗传学动物女(雌)性男(雄)性大鼠

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Synchronization of Ca²⁺-signals within insulin-secreting pseudoislets:: effects of gap junctional uncouplers

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CELL CALCIUM 2000年第5期27卷 287-296页

作者： Squires, PE Hauge-Evans, AC Persaud, SJ Jones, PM Kings Coll London Sch Biomed Sci Endocrinol & Reprod Res Grp London SE1 9RT England

The secretory response of the intact islet is greater than the response of individual beta-cells in isolation, and functional coupling between cells is critical in insulin release. The changes in intracellular Ca2+ ([Ca2+](i)) which initiate insulin secretory responses are synchronized between groups of cells within the islet, and gap-junctions are thought to play a central role in coordinating signalling events. We have used the MIN6 insulin-secreting cell line, to examine whether uncoupling gap-junctions alters the synchronicity of nutrient- and non-nutrient-evoked Ca2+ oscillations, or affects insulin secretion. MIN6 cells express mRNA species that can be amplified using PCR primers for connexin 36. A commonly used gap-junctional inhibitor, heptanol, inhibited glucose- and tolbutamide-induced Ca2+-oscillations to basal levels in MIN6 cell clusters at concentrations of 0.5 mM and greater, and it had similar effects in pseudoislets when used at 2.5 mM. Lower heptanol concentrations altered the frequency of Ca2+ transients without affecting their synchronicity, in both monolayers and pseudoislets. Heptanol also had effects on insulin secretion from MIN6 pseudoislets such that 1 mM enhanced secretion while 2.5 mM was inhibitory. These data suggest that heptanol has multiple effects in pancreatic beta-cells, none of which appears to be related to uncoupling of synchronicity of Ca2+ signalling between cells. A second gap-junction uncoupler, 18 alpha-glycyrrhetinic acid, also failed to uncouple synchronized Ca2+-oscillations, and it had no effect on insulin secretion. These data provide evidence that Ca2+ signalling events occur simultaneously across the bulk mass of the pseudoislet, and suggest that gap-junctions are not required to coordinate the synchronicity of these events, nor is communication via gap junctions essential for integrated insulin secretory responses. (C) Harcourt Publishers Ltd 2000.

关键词：投药局部消炎药/药理学钙信号/药物作用钙信号/生理学细胞系缝隙接合部/药物作用缝隙接合部/代谢葡萄糖/药理学甘草次酸/药理学庚醇/药理学降血糖药/药理学胰岛素/代谢胰岛/药物作用胰岛/代谢 RNA 信使/药物作用 RNA 信使/代谢甲苯磺丁脲/药理学动物人类小鼠

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Chronic carbon monoxide exposure in vivo induces myocardial endothelin-1 expression and hypertrophy in rat

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PHARMACOLOGY & TOXICOLOGY 1999年第4期85卷 192-197页

作者： Loennechen, JP Beisvag, V Arbo, I Waldum, HL Sandvik, AK Knardahl, S Ellingsen, O Norwegian Univ Sci & Technol Dept Physiol & Biomed Engn Med Tech Res Ctr N-7489 Trondheim Norway Natl Inst Occupat Hlth Dept Physiol N-0033 Oslo Norway

Smoking is associated with endothelial dysfunction and increased plasma levels of endothelin-l. The component of tobacco smoke inducing these effects is unknown. Carbon manoxide induces hypoxia, and there is evidence of carbon monoxide acting as a local mediator in both endothelial and smooth muscle cells. The purpose of this study was to determine whether chronic carbon monoxide exposure similar to that experienced by smokers affects myocardial endothelin-l expression. Sprague-Dawley female rats were exposed to carbon monoxide 100 ppm for one week or to 100 ppm for one week and 200 ppm for a second week. Carboxyhaemoglobin was 12+/-0.9% in the low and 23+/-1.1% in the high carbon monoxide exposure group. Endothelin-l expression was measured by competitive reverse transcriptase polymerase chain reaction. High carbon monoxide exposure increased endothelin-l mRNA by 54+/-12% (P<0.001) in the left ventricle and by 53+/-12% (P<0.001) in the right ventricle. In the low carbon monoxide exposure group corresponding changes were 43+/-14% (P=0.06) and 12+/-16% (P=0.29). Right ventricular weight increased by 18+/-7% (P=0.02) after high and by 16+/-5% (P=0.02) after low exposure. Left ventricular weight was elevated by 5+/-2% (P = 0.05) when both exposure groups were compared to controls. We conclude that chronic carbon monoxide exposure leading to carboxyhaemoglobin levels similar to those observed in smokers increases endothelin-l gene expression and induces myocardial hypertrophy in the rat.

关键词：一氧化碳/毒性碳氧血红蛋白/药物作用心脏扩大/化学诱导剂量效应关系药物内皮缩血管肽1/药物作用内皮缩血管肽1/代谢心室/药物作用心肌/代谢 RNA 信使/药物作用大鼠 Sprague-Dawley 逆转录聚合酶链反应动物女(雌)性大鼠

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Vascular smooth muscle cell proliferation and regrowth after mechanical injury in vitro are Egr-1/NGFI-A-dependent

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AMERICAN JOURNAL OF PATHOLOGY 1999年第3期155卷 897-905页

作者： Santiago, FS Atkins, DG Khachigian, LM Univ New S Wales Sch Pathol Ctr Thrombosis & Vasc Res Sch Pathol Sydney NSW 2052 Australia Johnson & Johnson Res Pty Ltd Sydney NSW Australia

Smooth muscle cell (SMC) proliferation is a key event in renarrowing of blood vessels after balloon angioplasty. Mechanical injury imparted to the arterial wall in experimental models induces the expression of the immediate-early gene, egr-1. Egr-1 binds to and activates expression from the proximal promoters of multiple genes whose products can, in turn, influence the vascular response to injury. Here, we used antisense strategies in vitro to inhibit rat vascular SMC proliferation by directly targeting Egr-1, A series of phosphorothioate antisense oligonucleotides of 15 base length and complementary to various theoretically accessible regions within Egr-1 mRNA were synthesized and assessed for their ability to selectively inhibit SMC proliferation in an Egr-1-dependent manner. Western blot analysis revealed that two oligonucleotides, AS2 and E11, inhibited Egr-1 synthesis in cells exposed to serum without affecting levels of the zinc finger protein Spl. AS2 and E11 inhibited serum-inducible [H-3]thymidine incorporation into DNA, as well as serum stimulation of total cell numbers. Size-matched phosphorothioate oligonucleotides with random, scrambled, sense or mismatch sequences failed to inhibit. Antisense Egr-1 inhibition was nontoxic and reversible. These oligonucleotides also inhibited SMC regrowth after mechanical injury in vitro. Egr-1 thus plays a key regulatory role in SMC proliferation and repair following injury.

关键词：结合部位血蛋白质类/药理学印迹法蛋白质细胞分裂/药物作用细胞培养的 DNA结合蛋白质类/拮抗剂和抑制剂 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/生理学早期生长反应蛋白质1 荧光素-5-异硫氰酸盐基因表达/药物作用即早蛋白质类显微镜检查荧光肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/损伤肌平滑血管/代谢核酸构象核酸合成抑制剂/药理学寡核苷酸类反义/代谢寡核苷酸类反义/药代动力学磷放射性同位素血小板源性生长因子/生物合成 RNA 信使/药物作用硫代核苷酸类/药代动力学硫代核苷酸类/药理学时间因素转录因子/拮抗剂和抑制剂转录因子/遗传学转录因子/生理学动物大鼠

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Attenuation and loss of hormonal modulation of KGF (FGF-7)/KGF receptor expression and mitogenesis during mammary tumor progression

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第2期184卷 222-228页

作者： Imagawa, W Pedchenko, VK Helber, J Xing, C Univ Kansas Med Ctr Dept Mol & Integrat Physiol Kansas City KS 66160 USA Univ Kansas Med Ctr Kansas Canc Inst Kansas City KS 66103 USA

Keratinocyte growth factor (KGF), alone and in synergism with progesterone (P) and prolactin (PRL), is mitogenic for normal mammary epithelium (ME) in vitro. In addition, P can upregulate ME sensitivity to KGF by slowing KGF receptor (KGFR) mRNA turnover in vitro. These hormonal interactions with KGF in vitro raise the possibility that alterations in these interactions can play a role in hormone-dependent mammary tumor growth and progression. The effect of hormones on KGF mitogenesis and the regulation of KGFR expression was examined in pregnancy-dependent (PDT) and ovarian-independent (OIT) mouse mammary tumors. In serum-free, collagen gel cell culture, dose/response (2-20 ng/ml) and time course studies showed that KGF stimulated the proliferation of PDT (not OIT) cells but synergism with P or PRL was not observed. The level of KGFR mRNA in PDT cells was not significantly different from normal ME but in OIT it was reduced more than 90%. P did not affect KGFR mRNA turnover in cultured PDT cells. However, KGFR mRNA was more stable in PDT cells compared to normal ME;after 6 days culture in basal medium, KGFR mRNA levels declined 40% vs. 85% previously shown for normal ME. Determination of KGF mRNA levels in tissues showed that it was lower in PDT compared to normal mammary gland and not detectable in OIT. These data show that in PDT both KGF-stimulated mitogenesis and the regulation of KGFR expression are independent of hormones. OIT has progressed to independence from any KGF influence. Thus, a subset of hormonally regulated pathways related to epithelial/stromal cell interactions can be lost in hormone-dependent mammary tumors during tumor progression. J. Cell. Physiol. 184:222-228, 2000. (C) 2000 Wiley-Liss, Inc.

关键词：细胞转化肿瘤/药物作用成纤维细胞生长因子10 成纤维细胞生长因子7 成纤维细胞生长因子生长物质/代谢生长物质/药理学角蛋白细胞/代谢乳腺动物/药物作用乳腺动物/代谢乳房肿瘤实验性/代谢有丝分裂原/生理学孕酮/药理学 RNA 信使/药物作用 RNA 信使/代谢受体成纤维细胞生长因子 2型受体成纤维细胞生长因子受体生长因子/代谢肿瘤细胞培养的动物女(雌)性人类小鼠妊娠

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Pyrrolidine dithiocarbamate prevents I-κB degradation and reduces microvascular injury induced by lipopolysaccharide in multiple organs

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MOLECULAR PHARMACOLOGY 1999年第4期55卷 658-667页

作者： Liu, SF Ye, XB Malik, AB Univ Illinois Coll Med Dept Pharmacol Chicago IL 60612 USA

Lipopolysaccharide (LPS) is a key mediator of multiple organ injury observed in septic shock. The mechanisms responsible for LPS-induced multiple organ injury remain obscure. In the present study, we tested the hypothesis that the LPS-induced injury occurs through activation of the transcription factor, nuclear factor-kappa B (NF-kappa B). We examined the effects of inhibiting NF-kappa B activation in vivo in the rat on LPS-induced: 1) gene and protein expression of the cytokine-inducible neutrophil chemoattractant (CINC) and intercellular adhesion molecule-1 (ICAM-1);b) neutrophil influx into lungs, heart, and liver;and c) increase in microvascular permeability induced by LPS in these organs. LPS (8 mg/kg, i.v.) challenge of rats activated NF-kappa B and induced CINC and ICAM-1 mRNA and protein expression. Pretreatment of rats with pyrrolidine dithiocarbamate (50, 100, and 200 mg/kg, i.p.), an inhibitor of NF-kappa B activation, prevented LPS-induced I-kappa B alpha degradation and the resultant NF-kappa B activation and inhibited, in a dose-related manner, the LPS-induced CINC and ICAM-1 mRNA and protein expression. Pyrrolidine dithiocarbamate also markedly reduced the LPS-induced tissue myeloperoxidase activity (an indicator of tissue neutrophil retention) and the LPS-induced increase in microvascular permeability in these organs. These results demonstrate that NF-kappa B activation is an important in vivo mechanism mediating LPS-induced CINC and ICAM-1 expression, as well as neutrophil recruitment, and the subsequent organ injury. Thus, inhibition of NF-kappa B activation may be an important strategy for the treatment of sepsis-induced multiple organ injury.

关键词：抗氧化剂/治疗应用毛细血管/病理学毛细血管通透性/药物作用趋化因子 CXC 趋化因子类/生物合成趋化因子类/遗传学 DNA结合蛋白质类/代谢酶抑制生长物质/生物合成生长物质/遗传学 I-κB蛋白质类胞间黏附分子1/生物合成胞间黏附分子1/遗传学胞间信号肽类和蛋白质类脂多糖类/毒性 NF-κB/代谢中性白细胞/药物作用中性白细胞/代谢过氧化物酶/代谢吡咯烷类/治疗应用 RNA 信使/生物合成 RNA 信使/药物作用大鼠 Sprague-Dawley 休克脓毒性/病理学硫代氨基甲酸酯类/治疗应用动物男(雄)性大鼠

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