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山东大学学报 (医学版) ›› 2019, Vol. 57 ›› Issue (5): 80-86.doi: 10.6040/j.issn.1671-7554.0.2019.021

• • 上一篇    

IL-1β介导的ERK通路对大鼠髁突软骨细胞外基质的作用

陈虹瑜1,2,曲竹丽3,孙琪4,赵华强1,5,马川1,5   

  1. 1. 山东省口腔组织再生重点实验室, 山东 济南 250012;2. 山东大学口腔医院急诊科, 山东 济南 250012;3. 山东医学高等专科学校口腔系, 山东 济南 250002;4. 济南市口腔医院口腔颌面外科, 山东 济南 250001; 5. 山东大学口腔医院口腔颌面外科, 山东 济南 250012
  • 发布日期:2022-09-27
  • 通讯作者: 赵华强. E-mail:zhaohq@sdu.edu.cn马川. E-mail: machuan@sdu.edu.cn
  • 基金资助:
    山东省自然科学基金(ZR2018PH022);山东省医药卫生科技发展计划(2017WS481)

Effects of interleukin-1β mediated ERK pathway on extracellular matrix of rat condylar chondrocytes

CHEN Hongyu1,2,QU Zhuli3, SUN Qi4, ZHAO Huaqiang1,5, MA Chuan1,5   

  1. 1. Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan 250012, Shandong, China;
    2. Department of Emergency, Stomatological Hospital of Shandong University, Jinan 250012, Shandong, China;
    3. Oral Department of Shandong Medical College, Jinan 250002, Shandong, China;
    4. Oral and Maxillofacial Surgery Department of Jinan Stomatological Hospital, Jinan 250001, Shandong, China;
    5. Department of Oral and Maxillofacial Surgery, Stomatological Hospital of Shandong University, Jinan 250012, Shandong, China
  • Published:2022-09-27

摘要: 目的 探讨白介素-1β(IL-1β)介导下细胞外调节蛋白激酶(ERK)通路对大鼠髁突软骨细胞外基质的作用。 方法 对Wistar大鼠髁突软骨细胞进行培养和鉴定。采用不同浓度的IL-1β处理髁突软骨细胞,检测ERK、Sry相关高速泳动族框因子9(Sox-9)、Ⅱ型胶原(COL2)的 mRNA表达,检测ERK、磷酸化ERK(P-ERK)、Sox-9、COL2的蛋白表达,并由此确定诱导细胞致炎且能激活ERK通路的最小IL-1β浓度;根据筛选的IL-1β浓度,将髁突软骨细胞随机分为3组:对照组、IL-1β组、IL-1β+ERK抑制剂组。检测各组ERK、Sox-9、COL2的mRNA表达及ERK、P-ERK、Sox-9和COL2的蛋白表达。 结果 培养传代的细胞形态与原代细胞相同,经免疫组化分析为髁突软骨细胞;用10ng/mL的IL-1β处理髁突软骨细胞,P-ERK的表达升高(P<0.05),Sox-9和COL2的表达降低(P<0.05);与IL-1β组比较, IL-1β+抑制剂组的P-ERK表达被抑制(P<0.05),Sox-9和COL2表达升高(P<0.05)结论 IL-1β能够通过激活ERK通路来抑制大鼠髁突软骨细胞Sox-9 和COL2的表达。

关键词: 髁突软骨细胞, 白介素-1β, 细胞外调节蛋白激酶信号通路, Sry相关高速泳动族框因子9, Ⅱ型胶原

Abstract: Objective To explore the effects of interleukin-1β mediated extracellular regulated protein kinases(ERK)pathway on extracellular matrix of rat condylar chondrocytes. Methods Condylar chondrocytes of Wistar rats were cultured and identified, which were then treated with different concentrations of IL-1β. The mRNA expressions of ERK, SRY-related high mobility group-box 9(Sox-9), type Ⅱ collagen(COL2), and the protein expressions of ERK, phosphorylated ERK(P-ERK), Sox-9 and COL2 were detected. The baseline IL-1β concentration which could induce cellular inflammation and activate ERK signaling pathway was determined. Based on the baseline IL-1β concentration, the 山 东 大 学 学 报 (医 学 版)57卷5期 -陈虹瑜,等.IL-1β介导的ERK通路对大鼠髁突软骨细胞外基质的作用 \=-condylar chondrocytes were divided into 3 groups: control group, IL-1β group and IL-1β+inhibitor group. The mRNA expression levels of ERK, Sox-9, COL2, and protein expression levels of ERK, P-ERK, Sox-9 and COL2 of all groups were detected. Results Cultured cells were identified as condylar chondrocytes by immunohistochemistry. The expression of P-ERK increased (P<0.05), while the expressions of Sox-9 and COL2 significantly decreased(all P<0.05)when treated with 10 ng/mL concentration of IL-1β. Compared with the IL-1β group, the IL-1β+inhibitor group had inhibited expression of P-ERK (P<0.05), but elevated expressions of Sox-9 and COL2(all P<0.05). Conclusion IL-1β is able to inhibit the expression levels of Sox-9 and COL2 by activating the ERK pathway of condylar chondrocytes.

Key words: Condylar chondrocytes, Interleukin-1β, Extracellular regulated protein kinases signaling pathway, SRY-related high mobility group-box 9, Type Ⅱ collagen

中图分类号: 

  • R782
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