Chinese Journal of Tissue Engineering Research ›› 2021, Vol. 25 ›› Issue (35): 5599-5603.doi: 10.12307/2021.287

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Inhibition of galectin-3 promotes apoptosis of cartilage endplate cells and induces intervertebral disc degeneration

Liu Yanlu, Hu Wei, Aikebaier, Yiliya, Huang Yifei   

  1. Hospital of Traditional Chinese Medicine Affiliated to Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region, China 
  • Received:2020-11-06 Revised:2020-11-11 Accepted:2021-01-23 Online:2021-12-18 Published:2021-08-03
  • Contact: Huang Yifei, MD, Chief physician, Hospital of Traditional Chinese Medicine Affiliated to Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region, China
  • About author:Liu Yanlu, MD candidate, Attending physician, Hospital of Traditional Chinese Medicine Affiliated to Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region, China
  • Supported by:
    the Natural Science Foundation of Xinjiang Uygur Autonomous Region, No. 2019D01C164 (to HW)

Abstract: BACKGROUND: Cartilage endplate degeneration of the intervertebral disc destroys the integrity of the intervertebral disc and impacts the exchange of nutrition and metabolites and the metabolic balance of extracellular matrix, which is the main factor leading to intervertebral disc degeneration. Galectin-3, a member of galectin family, is expressed in various tissues and participates in the regulation of cell proliferation, apoptosis, cell adhesion and other physiological and pathological processes. However, the regulatory role of Galectin-3 in the cartilage endplate of the intervertebral disc is still unclear.
OBJECTIVE: To investigate the effects of Galectin-3 on the proliferation, apoptosis and cell cycle of rat cartilage endplate cells through the intervention of GB1107, a Galectin-3 inhibitor.
METHODS: In this study, the rat cartilage endplate cells were divided into normal control group and Galectin-3 gb1107 inhibitor groups (1, 2.5, 5, 10, 25, and  50 μmol/L). MTT was used to detect the proliferation of cartilage endplate cells in each group at three time points (12, 24, 48 hours). The optimal concentration of 25 μmol/L was used for follow-up flow cytometry to detect the difference of cell apoptosis and cell cycle.
RESULTS AND CONCLUSION: The proliferation activity of chondrocytes treated with GB1107 was concentration- and time-dependent. In the concentration range of 5-50 μmol/L, the proliferation activity of chondrocytes was significantly lower than that of the normal control group at all three observational time points (P < 0.05). At the concentration of 25 μmol/L, the apoptosis rate of cartilage endplate cells was significantly higher than that of the normal control group (P < 0.05). Under the effect of GB1107, the number of cartilage endplate cells at G1 stage was significantly lower than that in the normal control group (P < 0.05), while the cell number at G2 and S stage was significantly lower than that in the normal control group (P < 0.05). Thererfore, inhibition of Galectin-3 may inhibit the DNA replication of cartilage endplate cells to promote the apoptosis of cartilage endplate cells and lead to the destruction of cartilage endplate, thereby inducing the occurrence and development of intervertebral disc degeneration.

Key words: Galectin-3, intervertebral disc degeneration, cartilage endplate, cell proliferation, cell apoptosis

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