Han F, Jiang H, Qu W, Rui Y-J
Soochow University, Suzhou, China.
Eur Rev Med Pharmacol Sci. 2020 Jun;24(12):6505-6516. doi: 10.26355/eurrev_202006_21634.
The purpose of this study was to explore the effects of Kruppel like factors 11 (KLF11) on oxidative stress, apoptosis, and endoplasmic reticulum stress (ERS) in osteoarthritis (OA) and its mechanism.
Human articular cartilage tissue was used to study the correlation between KLF11 and OA. Furthermore, human chondrocytes were used to explore the effects of KLF11 on oxidative stress, apoptosis, and ERS in chondrocytes by overexpressing KLF11 and using the OA inducer IL-1β. The p38MAPK signaling pathway agonist P79350 was used to study the effect of KLF11 on the p38 MAPK signaling pathway.
Articular cartilage tissue in OA patients and IL-1β-induced chondrocytes expressed higher KLF11. Overexpression of KLF11 significantly reduced oxidative stress levels, apoptosis levels, and activity of ERS-related pathways in chondrocytes. Moreover, P79350 attenuated the protective effect of KLF11 on chondrocytes by activating the p38MAPK signaling pathway.
KLF11 protects against OA by inhibiting oxidative stress, apoptosis, and ERS in chondrocytes by inhibiting p38MAPK signaling pathway.
本研究旨在探讨Kruppel样因子11（KLF11）对骨关节炎（OA）氧化应激、细胞凋亡和内质网应激（ERS）的影响及其机制。
用人关节软骨组织研究KLF11与OA的相关性。此外，通过过表达KLF11并使用OA诱导剂白细胞介素-1β（IL-1β），用人软骨细胞探讨KLF11对软骨细胞氧化应激、细胞凋亡和ERS的影响。使用p38丝裂原活化蛋白激酶（p38MAPK）信号通路激动剂P79350研究KLF11对p38 MAPK信号通路的影响。
OA患者的关节软骨组织和IL-1β诱导的软骨细胞中KLF11表达较高。KLF11的过表达显著降低了软骨细胞的氧化应激水平、细胞凋亡水平和ERS相关通路的活性。此外，P79350通过激活p38MAPK信号通路减弱了KLF11对软骨细胞的保护作用。
KLF11通过抑制p38MAPK信号通路，抑制软骨细胞的氧化应激、细胞凋亡和ERS，从而对OA起到保护作用。
