脂氧素抑制关节炎大鼠滑膜及IL-1β刺激的RSC-364细胞中VEGF的表达

周丹; 代洁; 艾青; 林玲; 张力

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脂氧素抑制关节炎大鼠滑膜及IL-1β刺激的RSC-364细胞中VEGF的表达

论著 | 更新时间：2026-01-09

- 脂氧素抑制关节炎大鼠滑膜及IL-1β刺激的RSC-364细胞中VEGF的表达
- Lipoxin suppresses VEGF expression in synovium of adjuvant arthritis rats and in interleukin 1β-stimulated RSC-364 cells
- 陆军军医大学学报 2015年37卷第21期页码：2121-2125
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  中图分类号： R322.72;R392.3;R977.6
- 纸质出版：2015
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周丹,代洁,艾青,林玲,张力.脂氧素抑制关节炎大鼠滑膜及IL-1β刺激的RSC-364细胞中VEGF的表达[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2121-2125.

　Zhou Dan,Dai Jie,Ai Qing,Lin Ling,Zhang Li.Lipoxin suppresses VEGF expression in synovium of adjuvant arthritis rats and in interleukin 1β-stimulated RSC-364 cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2121-2125.
周丹,代洁,艾青,林玲,张力.脂氧素抑制关节炎大鼠滑膜及IL-1β刺激的RSC-364细胞中VEGF的表达[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2121-2125. DOI：

　Zhou Dan,Dai Jie,Ai Qing,Lin Ling,Zhang Li.Lipoxin suppresses VEGF expression in synovium of adjuvant arthritis rats and in interleukin 1β-stimulated RSC-364 cells[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2121-2125. DOI：

摘要

目的探讨在体内外脂氧素A

（lipoxin A

，LXA

）对血管内皮生长因子（vascular endothelial growth factor，VEGF）表达的影响及其可能机制。方法 SD雄性大鼠（6~8周龄，200~250 g，32只）分为正常对照组、BML-111单独处理组（BML-111）、佐剂诱导的关节炎（adjuvant arthritis，AA）模型组及BML-111干预组（AA＋BML-111），每组8只。AA组通过左后足跖部注射弗氏完全佐剂诱导建立AA动物模型，AA+BML-111组于造模后每日腹腔注入LXA

受体激动剂BML-111。28 d后，取病变关节滑膜组织，匀浆后ELISA法检测VEGF水平，免疫印迹法检测VEGF受体2（VEGFR2）总蛋白水平及磷酸化水平。体外培养RSC-364大鼠成纤维样滑膜细胞（fibroblast-like synoviocyte，FLS），采用白细胞介素-1β（interleukin 1β，IL-1β）诱导VEGF表达，加入空白溶剂或不同浓度LXA

（1~100 nmol/L）共同孵育24 h后，ELISA法检测上清液中VEGF水平，免疫印迹法检测P38、JNK和ERK的总蛋白水平及磷酸化水平，免疫印迹法检测缺氧诱导因子-1α（hypoxia-inducible factors 1α， HIF-1α）蛋白含量。结果在AA大鼠滑膜组织，BML-111明显降低VEGF水平（P0.01），对VEGFR2表达无明显影响，但显著降低磷酸化VEGFR2的水平（P0.01）。在FLS细胞，LXA

剂量依赖性抑制IL-1β诱导的VEGF表达（P0.01），显著降低P38（P0.05）、JNK和ERK磷酸化水平（P0.01），下调HIF-1α含量（P0.01）。结论 LXA

可能通过抑制MAPK、HIF-1α下调RSC-364细胞中IL-1β诱导的VEGF表达，影响AA大鼠模型中血管新生和血管翳的形成。

Abstract

Objective To determine the effects of lipoxin A

(LXA

) on the expression of vas

cular endothelial growth factor (VEGF) in vivo and in vitro and investigate the possible underlying mechanism. Methods A total of 32 male SD rats (6 to 8 weeks old

weighing 200 to 250 g) were randomly and equally divided into 4 groups

that is

the normal control

BML-111 treatment group (LXA

receptor agonist)

adjuvant arthritis model group (AA)

and model plus BML-111 intervention group (AA＋BML-111). The AA model was induced by intradermal injection of complete Freund’s adjuvant into the left hind footpad of the rats. In the AA＋BML-111 group

the rats were supplemented with BML-111 daily for 28 d. Then the synovium from injured joints were harvested

the level of VEGF in the homogenates was determined by ELISA

and the total level and phosphorylated level of VEGF receptor 2 were determined by Western blot analysis. The rat fibroblast-like synoviocyte (FLS) RSC-364 was cultured in vitro and stimulated with interleukin-1β (IL-1β) in the absence or presence of LXA

(1 to 100 nmol/L) for 24 h. The concentrations of VEGF in the supernatant were determined by ELISA

the total levels and phosphorylated levels of p38

JNK and ERK

and the protein level of hypoxia-inducible factors 1α (HIF-1α) were determined by Western blotting. Results In the synovium from AA rats

LXA

down-regulated the generation of VEGF. It did not alter the total level of VEGFR2 but significantly suppressed the phosphorylation of VEGFR2. LXA

suppressed IL-1β-induced production of VEGF in FLS in a dose-dependent manner

reduced the levels of phosphorylated P38

JNK and ERK

and decreased the protein content of HIF-1α. Conclusion LXA

might down-regulate IL-1β-induced VEGF expression in RSC-364 cells via suppression of MAPK and HIF-1

which might regulate the angiogenesis and the formation of pannus during the progression of AA in rats

which may be a novel underlying mechanism of protective effects of LXA

on arthritis.

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