昆明医科大学学报2025，Vol.46Issue(6)：38-45,8.DOI:10.12259/j.issn.2095-610X.S20250605
基于lncRNA/Hedgehog信号通路表达探讨骨关节炎中自噬对软骨细胞凋亡的影响
Effects of Autophagy on Chondrocyte Apoptosis in Osteoarthritis:An Investigation Based on lncRNA/Hedgehog Signaling Pathway Expression
摘要
Abstract
Objective To investigate the effects of lncRNA/Hedgehog signaling pathway-mediated autophagy on chondrocyte function in osteoarthritis(OA).Methods Established an LPS-induced inflammatory chondrocyte model in OA chondrocytes(SW1353),and identified it through collagen Ⅱ immunofluorescence staining and toluidine blue staining,dividing the groups into Normal,LPS,LPS/lncRNA HHIP-AS1 inhibitor,and LPS/Scr groups.RT-qPCR was used to detect lncRNA HHIP-AS1 and HHIP expression in chondrocytes,Western blot was used to assess HHIP,Gli1,Gli2,LC3B-Ⅰ/Ⅱ,and p62 protein expression,TUNEL staining and flow cytometry(FC)were used to detect cell apoptosis,and immunofluorescence assay(IFA)was used to detect autophagy LC3B expression.Results When SW1 cells were treated with LPS,compared with normal chondrocytes,after LPS induction,the volume of chondrocytes increased,the number of vacuoli in the cytoplasm increased,the volume of the nucleus increased,the morphology of some cells was irregular,and the number relatively decreased.Toluidine blue staining and type Ⅱ collagen immunohistochemical staining decreased.LPS stimulation would induce cell death and autophagy.lncRNA HIP-AS1 and HHIP were upregulated(P<0.05),the key molecules of the Hedgehog signaling pathway HHIP,Gli1 and Gli2 were continuously upregulated(P<0.05),chondrocytes treated with LPS showed obvious apoptosis(P<0.05),and LC3B(green)accumulated.The biosynthesis and processing of LC3B increased(the levels of LC3B Ⅰ and Ⅱ increased),the degradation of p62 increased(P<0.05),and the lncRNA HIP-AS1 inhibitor reduced LPS-induced apoptosis of OA chondrocytes(decreased apoptosis rate)and autophagy(decreased autophagy rate of chondrocytes treated with LPS).The biosynthesis and processing of LC3B decreased(the levels of LC3B Ⅰ and Ⅱ decreased),and the degradation of p62 weakened),and the difference was statistically significant(P<0.05).Conclusion The lncRNA HHIP-AS1 may inhibit LPS-induced OA chondrocyte apoptosis and autophagy by regulating the Hedgehog signaling pathway.关键词
骨关节炎/lncRNA HHIP-AS1/Hedgehog/自噬/软骨细胞Key words
Osteoarthritis/lncRNA HIP-AS1/Hedgehog/Autophagy/Chondrocyte分类
医药卫生引用本文复制引用
朱毅琳,彭潇,张贵福,龙惠南..基于lncRNA/Hedgehog信号通路表达探讨骨关节炎中自噬对软骨细胞凋亡的影响[J].昆明医科大学学报,2025,46(6):38-45,8.基金项目
湖南省中医药管理局科研项目(C2024032) （C2024032）
长沙市中医药科研课题(B202301) （B202301）
