Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β‑ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β‑ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of β‑ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that β‑ecdysterone attenuated the apoptosis induced by tert‑butyl hydroperoxide via promoting autophagy in nucleus pulposus cells. Beclin‑1, an indispensable protein for the stimulation of autophagy, is upregulated and stabilized by β‑ecdysterone in a dose‑ and time‑dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3‑methyladenine partially abrogated the protective function of β‑ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β‑ecdysterone on IDD. Additionally, β‑ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β‑ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β‑ecdysterone may be a potential therapeutic agent for IDD.
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http://dx.doi.org/10.3892/mmr.2019.9861 | DOI Listing |
Cell Biochem Biophys
January 2025
Department of Orthopedic, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 430014, Hubei Province, China.
Intervertebral disc degeneration (IDD) is the main pathological factor resulting in low back pain (LBP), the leading cause of disability globally. Inflammatory response and extracellular matrix (ECM) degradation are critical pathological features in the development of IDD. Gastrodin (GAS), a phenol compound isolated from Gastrodia elata Blume, plays an anti-inflammatory role in experimental models of multiple human diseases.
View Article and Find Full Text PDFGen Physiol Biophys
January 2025
Department of Acupuncture, Chun'an County Traditional Chinese Medicine Hospital, Hangzhou, China.
Intervertebral disc degeneration (IVDD) is a common contributor for low back pain, which is featured by loss of extracellular matrix and nucleus pulposus cells (NPCs). Hence, our current study is undertaken to explore the potential mechanism of NPC apoptosis during IVDD. Transcription factor Dp-1 (TFDP1) expression in degenerative and non-degenerative intervertebral disc tissues was analyzed by bioinformatics.
View Article and Find Full Text PDFBiochem Biophys Rep
March 2025
Orthopedics of TCM Senior Department, The Sixth Medical Center of PLA General Hospital, Beijing, 100048, China.
Background: Intervertebral disc degeneration (IVDD) has been linked to ferroptosis, a type of programmed cell death. The role of platelet-rich plasma (PRP) in mitigating ferroptosis in nucleus pulposus (NP) cells within IVDD remains unclear.
Purpose: This study aims to verify the effectiveness of PRP in reducing ferroptosis in NP cells induced by Erastin.
Adv Sci (Weinh)
January 2025
Department of Orthopedic Surgery, Changzheng Hospital, Naval Medical University, Shanghai, 200003, P. R. China.
Nucleus pulposus cell (NPC) senescence contributes to intervertebral disc degeneration (IVDD). However, the underlying molecular mechanisms are not fully understood. In this study, it is demonstrated that angiotensin-converting enzyme 2 (ACE2) counteracted the aging of NPCs and IVDD at the cellular and physiological levels.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Department of Orthopedic Surgery and Orthopedic Research Institute, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
The progression of intervertebral disc degeneration (IVDD) is associated with increased cell apoptosis and reduced extracellular matrix (ECM) production, both of which are driven by ongoing inflammation. Thus, alleviating the acidic inflammatory microenvironment and mitigating the apoptosis of nucleus pulposus cells (NPCs) are essential for intervertebral disc (IVD) regeneration. Regulating pH levels in the local environment can reduce inflammation and promote tissue recovery.
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