Volume 46 Issue 6
Jun.  2025
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Yilin ZHU, Xiao PENG, Guifu ZHANG, Huinan LONG. Effects of Autophagy on Chondrocyte Apoptosis in Osteoarthritis: An Investigation Based on lncRNA/Hedgehog Signaling Pathway Expression[J]. Journal of Kunming Medical University, 2025, 46(6): 38-45. doi: 10.12259/j.issn.2095-610X.S20250605
Citation: Yilin ZHU, Xiao PENG, Guifu ZHANG, Huinan LONG. Effects of Autophagy on Chondrocyte Apoptosis in Osteoarthritis: An Investigation Based on lncRNA/Hedgehog Signaling Pathway Expression[J]. Journal of Kunming Medical University, 2025, 46(6): 38-45. doi: 10.12259/j.issn.2095-610X.S20250605

Effects of Autophagy on Chondrocyte Apoptosis in Osteoarthritis: An Investigation Based on lncRNA/Hedgehog Signaling Pathway Expression

doi: 10.12259/j.issn.2095-610X.S20250605
  • Received Date: 2024-11-29
  • Publish Date: 2025-06-25
  •   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.
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