|本期目录/Table of Contents|

[1]李艳芬,许雯静,吴春芳,等.IL-10拮抗Pg-LPS所致高脂血症兔枯否氏细胞炎症反应的实验研究[J].福建医科大学学报,2016,50(06):359-364.
 LI Yanfen,XU Wenjing,WU Chunfang,et al.Experimental Study of IL-10 anta Ponizing Inflammatory Reactionof Kuffer Cell Induced by Pg-LPS in Hyperlipidemia Rabbit[J].Journal of Fujian Medical University,2016,50(06):359-364.
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IL-10拮抗Pg-LPS所致高脂血症兔枯否氏细胞炎症反应的实验研究(PDF)
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《福建医科大学学报》[ISSN:1672-4194/CN:35-1192/R]

卷:
第50卷
期数:
2016年06期
页码:
359-364
栏目:
论著
出版日期:
2016-12-30

文章信息/Info

Title:
Experimental Study of IL-10 anta Ponizing Inflammatory Reactionof Kuffer Cell Induced by Pg-LPS in Hyperlipidemia Rabbit
文章编号:
1672-4194(2016)06-0359-06
作者:
李艳芬1许雯静2吴春芳1游晓庆1骆 凯1闫福华3
1.福建医科大学 附属口腔医院牙周科,福州 350002;
2.福建省人民医院 口腔科,福州 350004;
3.南京大学医学院 附属口腔医院,南京 210008
Author(s):
LI Yanfen1 XU Wenjing2WU Chunfang1 YOU Xiaoqing1 LUO Kai1YAN Fuhua3
1.Department of Periodontology,School and Hospital of Stomatology, Fujian Medical University, Fuzhou 350002, China;
2.Department of Stomatology, People’s Hospital of Fujian Province, Fuzhou 350004, China;
3. Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China
关键词:
*卟啉单胞菌 牙髓 脂多糖类 白细胞介素10 高脂血症 炎症
Keywords:
porphyromonas endodontalis lipopolysaccharides interleukin-10 hyperlipidemias inflammation
分类号:
R332; R378.84; R392.12; R977
DOI:
-
文献标志码:
A
摘要:
目的 探讨白细胞介素-10(IL-10)对牙龈卟啉单胞菌脂多糖(Pg-LPS)引起的高脂血症兔肝脏枯否氏细胞(KC)炎症反应的影响。 方法 健康新西兰兔12只随机分为2组,分别喂予基础饲料和高脂饲料。喂养6周后建立高脂血症模型。分离、收集KC,将正常和高脂组KC随机分为:对照组、Pg-LPS组(1 μg/mL Pg-LPS刺激)、IL-10+Pg-LPS组(0.1 μg/mL IL-10+1 μg/mL Pg-LPS刺激)。刺激24 h后,采用Griess法检测NO,Western-blot法检测NF-κB p65及IκB-α,DCFH-DA荧光检测细胞内ROS的表达。 结果 对照组中高脂KC的NF-κB p65蛋白及NO,ROS水平均高于正常KC。Pg-LPS作用后,正常及高脂KC的炎症物质表达量升高,且高脂血症与Pg-LPS呈协同作用。IL-10的干预处理使NO,ROS,NF- κB p65表达下降,IκB-α表达升高,对Pg-LPS所引起的炎症反应起抑制作用,对高脂KC的抑制作用更加明显。 结论 高脂血症可使KC处于相对激活状态。在牙周致病菌Pg-LPS作用下,高脂血症和Pg-LPS具有协同作用,IL-10可抑制Pg-LPS所致KC的炎性反应,且对高脂状态下KC的干预作用更佳。
Abstract:
Objective To explore the effect of interleukin-10 on inflammatory reaction of Kuffer cell following the Pg-LPS stimulation in hyperlipidemia rabbit. Methods 12 New Zealand rabbits were randomly divided into two groups and were fed with normal or high fat diet. The hyperlipidemia model was established 6 weeks later. We isolated and cultured the Kuffer cells(KC). Both normal and hyperlipidemia group were divided into 3 groups: control, Pg-LPS at 1 μg/mL, and Pg-LPS at 0.1 μg/mL IL-10+1 μg/mL. After the treatment for 24 h, NO levels were detected by Griess assay. NF-κB p65 and IκB-α fragment were inspected by Western blot. ROS levels were determined by fluorescence enzyme-labelled meter with DCFH-DA as fluorescent probe. Results The levels of NF-κB p65,NO and ROS were higher in hyperlipidemia control group than in normal control group. After being stimulated by Pg-LPS, the expression of inflammatory substances was increased indicating a synergistic effect between hyperlipidemia and Pg-LPS. Under the IL-10 treatment the expression of NO,ROS,NF-κB p65 were decreased, while the expression of IκB-α was increased. IL-10 inhibited the inflammatory reaction induced by Pg-LPS, and the inhibition was more significant in the KC of hyperlipidemia rabbit. Conclusion The KC of hyperlipidemia rabbit is in a relatively activated condition, after being stimulated by Pg-LPS, hyperlipidemia and Pg-LPS present a synergistic effect. IL-10 can inhibit the inflammatory reaction of KC after the Pg-LPS stimulation, and the effect is better for the KC with hyperlipidemia.

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备注/Memo

备注/Memo:
基金项目: 国家自然科学基金(30973326); 福建省自然科学基金(2013J01306); 福建省教育厅科研基金(JA11123)
作者简介: 李艳芬(1979-),女,副主任医师,医学博士
通讯作者: 闫福华. Email: fhyan2005@126.com
更新日期/Last Update: 2016-12-25