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| 1 | Acanthopanax senticosus polysaccharides-induced intestinal tight junction injury alleviation via inhibition of NF-κB/MLCK pathway in a mouse endotoxemia model显示文摘AIM To examine the effects of Acanthopanax senticosus polysaccharides(ASPS) on intestinal tight junction(TJ) disruption and nuclear factor-kappa B(NF-κB)/myosin light chain kinase(MLCK) activation in endotoxemia.METHODS BALB/C mice(6-8-weeks-old) received continuous intragastric gavage of ASPS for 7 d before injection of lipopolysaccharide(LPS), or received ASPS once after LPS injection. Blood and intestinal mucosal samples were collected 6 h after LPS challenge. Clinical symptoms, histological injury, intestinal permeability,TJ ultrastructure, and TJ protein expression were determined.RESULTS Compared with mice in the LPS group, pretreatment with ASPS improved clinical and histological scores by 390.9%(P < 0.05) and 57.89%(P < 0.05), respectively, and gut permeability change in endotoxemic mice was shown by a 61.93% reduction in reduced leakage of fluorescein isothiocyanate-dextran 6 h after LPS injection(P < 0.05). ASPS pretreatment also prevented LPS-induced TJ ultrastructure breakdown supported by increased electron dense materials between adjoining cells, sustained redistribution and expression of occludin(0.597 ± 0.027 vs 0.103 ± 0.009, P < 0.05) and zonula occludens-1(0.507 ± 0.032 vs 0.125 ± 0.019, P < 0.05), and suppressed activation of the NF-κB/MLCK pathway indicated by reduced expression of NF-κB, phospho-inhibitor kappa B-alpha, MLCK and phospho-myosin light-chain-2 by 16.06%(P < 0.05), 54.31%(P < 0.05), 66.10%(P < 0.05) and 64.82%(P < 0.05), respectively. CONCLUSION ASPS pretreatment may be associated with inhibition of the NF-κB/MLCK pathway and concomitant amelioration of LPS-induced TJ dysfunction of intestinal epithelium in endotoxemia. | Jie Han Ji-Hong Li Guang Bai Guo-Shun Shen Jing Chen Jia-Nan Liu Shuo Wang Xian-Jun Liu | 2017 | World Journal of Gastroenterology2017，23，12： | 11 |
| 2 | 内皮分化基因受体介导溶血磷脂酸:肿瘤靶向治疗的新靶点显示文摘溶血磷脂酸(lysophosphatidic acid,LPA)是一种对多种细胞具有不同生物学活性的磷脂介质,在组织中广泛存在。从细胞形态学改变到细胞功能的影响,LPA可产生如促进细胞增殖、迁移和耐药等生物学效应。如其他生物递质一样,LPA与细胞表面特定的G蛋白偶合受体(G protein-coupled receptoi,GPCR)发生交联作用,这些受体主要有Edg-2/LPA1、Edg-4/IPA2和Edg-7/LPA3等,它们被命名为内皮分化基因或溶血磷脂受体亚家族(endothelial differentiation gene or lysophospholipid receptor subfamily,Edg/LPAR subfamily)。LPA在体内外参与细胞增殖以及血管生成等病理生理过程,LPA代谢和Edg/LPA受体功能的异常与肿瘤的发生、发展相关,可能是肿瘤临床诊治的潜在靶点。本文阐述了LPA通过Edg/LPA受体介导在肿瘤发生和发展中的作用及其机制,并就其在胰腺癌临床诊治中的意义进行了评价。 | 龚涌灵 Frank FANG | 2011 | 中国肿瘤生物治疗杂志2011，18，6： | 3 |
| 3 | Expression of lysophosphatidic acid and its receptor in human pancreatic cancer and its clinical evaluation of diagnosis and therapy显示文摘 | WANGShao-kai TAOChen-jie WANGWei-dong LUGuang-mei GONGYong-ling | 2011 | 东南大学学报(医学版)2011，30，5： | 2 |
| 4 | 溶血磷脂酸在消化系肿瘤中的作用显示文摘溶血磷脂酸是一种细胞间磷脂类信号分子,通过G蛋白偶联受体参与多种肿瘤的发生和发展,本文就溶血磷脂酸的结构及生物学作用在消化系肿瘤发生、发展中的作用机制进行探讨. | 钟月圆 黄杰安 | 2010 | 世界华人消化杂志2010，18，3： | 1 |
| 5 | 己酮可可碱抑制人卵巢癌HO-8910PM细胞AnnexinⅡ、NF-κB p65蛋白的表达显示文摘目的观察己酮可可碱(PTX)对体外培养的人卵巢癌细胞增殖及其AnnexinⅡ、NF-κB p65蛋白表达的影响。方法不同浓度PTX作用于人卵巢癌细胞HO-8910PM,采用四甲基偶氮唑蓝(MTT)比色法检测其对HO-8910PM增殖的影响;采用免疫细胞化学方法检测PTX作用前后HO-8910PM细胞AnnexinⅡ、NF-κBp65蛋白表达的变化。结果 MTT结果显示:不同浓度PTX(0.25~2.0mg/ml)作用于HO-8910PM细胞12、24、48、72h,均可不同程度抑制细胞增殖,同一时间段各浓度PTX作用组与空白对照组相比差异有统计学意义(P<0.05),各浓度PTX作用组组内两两相比差异有统计学意义(P<0.05)。PTX同一浓度组各时间点两两相比细胞增殖抑制率差异均有统计学意义(P<0.05)。免疫细胞化学显示:以不同浓度的PTX(0.5~2.0mg/ml)作用HO-8910PM细胞24、48、72h后,AnnexinⅡ蛋白较空白对照组有所降低;同一时间段内AnnexinⅡ蛋白表达呈浓度依赖性,差异有统计学意义(P<0.05),同一剂量组AnnexinⅡ蛋白表达呈时间依赖性,差异有统计学意义(P<0.05)。不同浓度PTX(0.5~2.0mg/ml)作用于HO-8910PM细胞24、48、72h后,NF-κBp65蛋白的表达均有所降低,也呈时间和浓度依赖性,差异有统计学意义(P<0.05)。结论 PTX可能通过抑制HO-8910PM卵巢癌细胞AnnexinⅡ、NF-κBp65蛋白表达而抑制其增殖。 | 谷晓广 李道明 | 2010 | 第二军医大学学报2010，31，6： | 0 |
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