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| 雷公藤红素对IL-1β致软骨终板退变的影响 |
| The influence of celastrol on cartilage endplate degeneration of intervertebral disc induced by IL-1β |
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| DOI：10.3969/j.issn.1006.7108.2017.12.020 |
| 中文关键词: 雷公藤红素 IL-1β 金属蛋白酶 软骨终板细胞 |
| 英文关键词:Celastrol IL-1β Matrix metalloproteinases Chondrocytes of the endplate |
| 基金项目:南京市科技局课题（2014sc513010） |
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| 中文摘要: |
| 目的 通过IL-1β与雷公藤红素体外刺激小鼠椎间盘软骨终板细胞，探讨雷公藤红素能否抑制IL-1β对软骨终板细胞的影响。方法 不同浓度的雷公藤红素刺激软骨终板细胞，CCK-8法检测不同时间点其对软骨终板细胞增殖作用的影响；实验共分3组：空白对照组（无血清DMEM培养基），IL-1β诱导组（IL-1β 5 ng/mL共同孵育2 h），雷公藤红素干预组（经IL-1β 5 ng/mL共同孵育2h后，再以雷公藤红素共同孵育24 h）。分组处理后，ELISA法检测MMP-1、MMP-3的水平，同时荧光定量PCR检测蛋白多糖及II胶原的mRNA表达水平。结果 与空白对照组相比，IL-1β刺激软骨终板细胞2h后，MMP-1、MMP-3表达水平明显增高，雷公藤红素可抑制细胞中IL-1β介导的MMP-1、MMP-3的表达，同时IL-1β明显抑制软骨终板细胞的蛋白多糖及II胶原mRNA的表达，而雷公藤红素可上调IL-1β诱导的蛋白多糖及II胶原mRNA的表达水平。结论 雷公藤红素能够抑制IL-1β介导的软骨终板退变进程，上调蛋白多糖及II胶原mRNA的表达水平，可能在防治椎间盘退变性疾病中发挥重要作用。 |
| 英文摘要: |
| Objective We aimed to explore the potential mechanism of Celastrol in suppressing the influence of IL-1β on endplate chondrocytes through stimulating chondrocytes of the endplate using IL-1β and Celastrol in vitro. Methods Chondrocytes of the endplate were induced by different concentrations of Celastrol. The proliferation of chondrocytes of the endplate was determined by CCK-8 assays. The chondrocytes of the endplate were divided into control group with complete medium, IL-1β-induced group with 5 ng/mL IL-1β of complete medium for 2 h and Celastrol treatment group with Celastrol for 24 h after being added with 5 ng/mL IL-1β of complete medium for 2 h. MMP-1 and MMP-3 were measured by ELISA after chondrocytes of the endplate induced by IL-1β and Celastrol, and mRNAs of proteoglycan and type II collagen were assessed by RT-qPCR. Results The expression levels of MMP-1 and MMP-3 were significantly upregulated in chondrocytes of the endplate induced by IL-1β for 2h compared with the blank control, and the effect was markedly inhibited by Celastrol. Moreover, the expression levels of proteoglycan and type II collagen were significantly suppressed in chondrocytes of the endplate induced by IL-1β for 2h compared with the blank control, and Celastrol could upregulated the expression of proteoglycan and type II collagen. Conclusions Celastrol may effectively inhibit the degeneration process of cartilage endplate induced by IL-1β, contribute to the expression of proteoglycan and type II collagen, and play an important role in the suppression of degenerative disc disease. |
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