| 梁爽,鲁锐,何直益,何琰泽,杨卿.敲低RIPK1抑制软骨细胞衰老水平延缓OA病理进展.[J].中南医学科学杂志.,2023,(2):161-165. |
| 敲低RIPK1抑制软骨细胞衰老水平延缓OA病理进展 |
| Knocking down RIPK1 delays the pathological progression of OA by inhibiting chondrocyte aging level |
| 投稿时间：2022-09-17 修订日期：2023-01-28 |
| DOI：10.15972/j.cnki.43-1509/r.2023.02.002 |
| 中文关键词: 骨关节炎 软骨细胞 衰老 RIPK1 [ |
| 英文关键词:osteoarthritis chondrocyte senescence RIPK1 |
| 基金项目:国家自然科学基金(81601951) |
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| 中文摘要: |
| 目的探讨受体相互作用丝氨酸/苏氨酸激酶1(RIPK1)对骨关节炎(OA)病理进展的影响。 方法将软骨细胞分为对照组(NC组)、白细胞介素-1β组(IL-1β组)和IL-1β+RIPK1短发夹RNA腺病毒载体组(IL-1β+sh-RIPK1组)。使用5 μg/L IL-1β刺激小鼠原代软骨细胞,同时使用腺病毒敲低RIPK1表达,检测软骨细胞炎症指标和衰老表型变化。在体内实验中,构建小鼠OA模型,同时使用腺病毒敲低关节软骨中RIPK1的表达,通过免疫印迹、衰老相关-β-半乳糖苷酶(SA-β-Gal)染色和qRT-PCR观察小鼠膝关节病理进展和衰老表型。 结果在体外细胞实验中,IL-1β刺激能显著上调软骨细胞炎症表型。敲低RIPK1表达后,软骨细胞炎症表型受到明显抑制,且软骨细胞衰老表型也显著下调(P＜0.05)。同时,体内动物实验也得到了相同的结果。 结论敲低RIPK1抑制软骨细胞衰老水平延缓OA病理进展。 |
| 英文摘要: |
| AimTo investigate the effect of receptor-interacting serine/threonine kinase 1 (RIPK1) on the progression of osteoarthritis (OA) cases. MethodsChondrocytes were divided into blank control group (NC), interleukin-1β group (IL-1β group) and IL-1β+RIPK1 short hairpin RNA adenovirus vector group (IL-1β+sh-RIPK1 group). Primary chondrocytes were stimulated with IL-1β, and the expression of RIPK1 was knocked down by adenovirus. The expression levels of inflammatory markers and aging genes were detected in chondrocytes. In vivo, the OA model was constructed, and the RIPK1 expression in articular cartilage was knocked down by adenovirus. The pathological progression, SA-β-Gal staining and senescence associated genes were observed by western blotting and qRT-PCR. ResultsIn vitro cell experiment, IL-1β stimulation can significantly up-regulate the inflammatory phenotype of chondrocytes, However, after RIPK1 knockdown, the expression levels of inflammatory markers were significantly downregulated, and the aging phenotype of chondrocytes was also significantly down-regulated (P＜0.05). At the same time, the same results were obtained in vivo animal experiments. ConclusionKnocking down RIPK1 delays the pathological progression of OA by inhibiting chondrocyte aging level. |
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