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| 1 | Synthesis of endotoxin receptor CD14 protein in Kupffer cells and its role in alcohol-induced liver disease显示文摘AIM: To observe the synthesis of endotoxin receptor CD14 protein and its mRNA expression in Kupffer cells (KCs), and evaluate the role of CD14 in the pathogenesis of liver injury in rats with alcohol-induced liver disease (ALD).METHODS: Twenty-eight Wistar rats were divided into two groups: ethanol-fed group and control group. Ethanol-fed group dextrose instead of ethanol. Two groups were sacrificed at 4 wk and 8 wk, respectively. KCs were isolated and the synthesis of CD14 protein and its mRNA expression in KCs were determined by flow cytometric analysis (FCM)or the reverse transcription polymerase chain reaction (RTPCR) analysis. The levels of plasma endotoxin and alanine transaminase (ALT) were measured by Limulus Amebocyte Lysate assay and standard enzymatic procedures respectively, and the levels of plasma tumor necosis factor (TNF)-α and interleukin (IL)-6 were both determined by ELISA. The liver pathology change was observed under light and electric microscopy.RESULTS: In ethanol-fed group, the percentages of FITCCD14 positive cells were 76.23 % and 89.42 % at 4 wk and 8 wk, respectively. Compared with control group (4.45 %and 5.38 %), the difference was significant (P<0.05). The expressions of CD14 mRNA were 7.56±1.02 and 8.74±1.37 at 4 wk and 8 wk, respectively, which were significantly higher compared with the control group (1.77±0.21 and 1.98±0.23)(P<0.05). Plasma endotoxin levels at 4 wk and 8 wk increased dramatically in ethanol-fed rats (112±15 IU/L and 147±22 IU/L) than those in the control animals (31±12 IU/L and 33±9 IU/L) (P<0.05). In ethanol-fed rats, the levels of wk, respectively which were significantly higher than those fed rats, there were marked pathological changes including steatosis, cell infiltration and necrosis. No marked pathological changes were seen in control group.CONCLUSION: Ethanol administration led to a significantsynthesis of endotoxin receptor CD14 protein and its gene expression in KCs, which maybe result in the pathological changes of liver tissue and hepatic functional damages. | Li-LiDai Jian-PingGong Guo-QingZuo Chuan-XinWu Yu-JunShi Xu-HongLi YongPeng WuDeng Sheng-WeiLi chang-AnLiu | 2003 | World Journal of Gastroenterology2003，9，3： | 20 |
| 2 | Intestinal damage mediated by Kupffer cells in rats with endotoxemia显示文摘AIM: To determine the in vivo effects of phagocytic blockadeof Kupffer cell (KC) on the release of proinflammatorycytokines in small intestinal lesion and on the integrity ofintestinal tract by using gadolinium chloride (GdCI3) duringearly endotoxemia.METHODS: Wistar rats were divided into three groups: GroupA, rats were injected with endotoxin (F. coli O111:B4, a doseof 12 mg.kg-1) only; Group B, rats were pretreatedintravenously with 25 mg of GdCl3 per kg 24 h are givenendotoxin; and Group C, sham operation on ly.All animalswere sacrificed 4 h after endotoxin injection.Mn portion ofthe rats of three groups, bile duct was cannulated, which thebile was collected externally. Morphological changes of ileumwere observed under light microscopy and electronicmicroscopy. The KC were isolated from rats by collagenaseperfusion and in KC, expression of TNF-α and IL-6 mRNAwere determined by RT-PCR analysis. Plasma and bile TNF-αand IL-6 Levels were determined by enzyme-linkedimmunosorbent assay (ELISA).RESULTS: In group A, there were neutrophil infiltrationand superficial epithelial necrosis of the ileal villi, sloughingof mucosal epithelium, and disappearance of some villi. Ingroup B, the ileal mucosal damage was much reduced. whichin group C, no significant morphological changes were seen.GdCl3 pretreatment decreased significantly the expressionof TNF-α and IL-6 mRNA in group B (4.32±0.47 and 4.05±0.43) when compared to group A (9.46±1.21 and 9.04±1.09) (P<0.05). There was no significant expression of TNF-α and IL-6 mRNA in group C (1.03±0.14 and 10.4±0.13).In rats of group A, the levels of TNF-α and IL-6 in bile andplasma were 207±29 ng. L-1, 1032±107 ng. L-1, 213±33ng. L-1, and 1185±127 ng. L-1, respectively. In group B, theywere 113±18 ng. L-1, 521±76 ng. L-1, 147±22 ng. L-1, and572±54 ng. L-1, respectively. In group C, they were 67±10ng. L-1, 72±13 ng. L-1, 109±18 ng. L-1, and 118±22 ng. L-1respectively. There were significant difference between thethree group (P | Jian-PingGong Chuan-XinWu | 2002 | World Journal of Gastroenterology2002，8，5： | 15 |
| 3 | 慢性肾功能不全与动脉粥样硬化显示文摘 | 王海涛 彭佑铭 | 2002 | 临床肾脏病杂志2002，2，2： | 5 |
| 4 | A novel point mutation in CD18 causing leukocyte adhesion deficiency in a Chinese patient显示文摘( LAD-1 )背景白血球粘附缺乏类型 1 是周期性的严重细菌的感染描绘的稀罕、正染色体的后退的继承免疫不全疾病,损害的脓形成,差的创伤愈合,在为白细胞的能力负责的 CD18 基因与变化联系了向 inflammation.Correct 和 LAD-1 的早诊断的地点从血溪流移居对治疗的成功和这的好攻击的 infections.The | LI Li JIN Ying-ying CAO Rui-ming CHEN Tong-xin | 2010 | Chinese Medical Journal2010，，10： | 4 |
| 5 | ACS患者体内同型半胱氨酸与黏附分子CD11b/CD18的相关性显示文摘目的:探讨急性冠脉综合征患者体内血浆同型半胱氨酸(HCY)与全血白细胞黏附分子CD11b/CD18水平的变化及其相关性。方法:对急性冠脉综合征(ACS)患者53例与健康人35例采用酶联免疫法测定血浆HCY水平,通过流式细胞仪采用直接免疫荧光法测定白细胞黏附分子CD11b/CD18的表达。结果:ACS组血浆HCY水平显著高于对照组,分别为29.1±13.5和12.7±6.9μmol/L(P<0.01),ACS组白细胞表面CD11b/CD18表达水平显著高于对照组,分别为6.0±2.3比4.3±1.6 MFI(P<0.05),27.7±7.7比19.6±4.9 MFI(P<0.05)。HCY水平与CD11b、CD18的表达显著相关。结论:同型半胱氨酸作为炎症介质可能通过调节白细胞黏附分子CD11b/CD18的表达,在ACS发生和发展中起重要作用。 | 杨泉 郭雪微 阿祥仁 徐义先 谢萍 施一凡 | 2005 | 心脏杂志2005，17，4： | 1 |
| 6 | 急性冠状动脉综合征病人同型半胱氨酸和黏附分子的改变显示文摘目的探讨急性冠状动脉综合征(acute coronary syndrome,ACS)病人体内血浆同型半胱氨酸(homocysteine,Hcy)、分化群(cluster of differentiation antigen,CD)11b/CD18、C反应蛋白(C-reactive protein,CRP)和白细胞计数的改变。方法选择ACS75例、稳定型心绞痛(stabe angina pectoris,SAP)35例,健康人35名为对照组,用酶联免疫法测定血浆Hcy,采用直接免疫荧光法用流式细胞仪测定CD11b与CD18表达,比较CRP、白细胞计数、血糖、血脂和血压改变。结果①ACS组和SAP组的血糖、总胆固醇、低密度脂蛋白-胆固醇均高于对照组,而高密度脂蛋白胆固醇则低于对照组;而在ACS组和SAP组差异无统计学意义;ACS组收缩压和舒张压均高于对照组;②ACS组血浆Hcy(19±11)#mol/L、CD11b和CD18表达分别为(6.0±2.3)MC(平均荧光强度单位)和(27.7±4.3)MC,白细胞计数为(9.4±2.4)×109/L均高于SAP组(P<0.05)。CRP为3.75(0.5~7)mg/L,与SAP组比较,差异无统计学意义;SAP与对照组比较,仅Hcy轻度升高和CRP升高,余差异无统计学意义。结论ACS和SAP有血脂、血糖、血压改变,同时Hcy、白细胞计数及CD、CRP升高,表明炎性因素可能参与冠心病的发生。 | 王雪里红 郭雪微 杨泉 | 2007 | 岭南心血管病杂志2007，13，5： | 0 |
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