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| Exploring the mechanism of Qishe Pills and its active component in delaying intervertebral disc degeneration and nucleus pulposus cell senescence：A study based on network pharmacology and experimental validation |
| Hits 86 Download times 61 Received:December 26, 2025 |
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| DOI
10.11656/j.issn.1673-9043.2026.06.10 |
| Key Words
intervertebral disc degeneration;Qishe Pills;network pharmacology;p53 signaling pathway;in vitro experiments |
| Author Name | Affiliation | E-mail | | ZHANG Cheng | Spine Disease Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China | | | WANG Bingquan | Department of Acupuncture and Moxibustion Tuina Traumatolog, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200032, China | | | DAI Yuxiang | Department of Orthopedics, Suzhou TCM Hospital affiliated to Nanjing University of Traditional Chinese Medicine, Suzhou 215009, China | | | WANG Yongjun | Spine Disease Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China | | | SUN Yueli | Spine Disease Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China | yueli_sun@foxmail.com |
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| Abstract
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| [Objective] To investigate the mechanism by which Qishe Pills（QSP） and its effective components delay intervertebral disc degeneration（IVDD） and nucleus pulposus（NP） cell senescence，utilizing network pharmacology and experimental validation. [Methods] Active components of QSP and their potential targets were screened based on network pharmacology，and a “Component-Target-Pathway” network was constructed. The binding affinity between active components of QSP and key targets of relevant signaling pathways was validated by molecular docking. Combined with in vitro experiments，an NP cell senescence model was established. Effective monomers were identified，and the upstream-downstream relationships of their action pathways were explored using Western blot and immunofluorescence assays. [Results] Network pharmacology revealed that the intersection targets were significantly enriched in the p53 signaling pathway and were associated with the PI3K/AKT，AMPK/SIRT1，ERK，and TGF-β/Smad pathways. Molecular docking and experimental validation identified tetrandrine as the effective component of QSP regulating IVDD. In vitro experiments confirmed that tetrandrine inhibits p53 pathway activity via the upstream PI3K/AKT/MDM2 pathway，thereby reducing NP cell apoptosis and promoting the synthesis of type II collagen（COL2A1）. [Conclusion] NP cell senescence is a key pathological factor in IVDD. This study elucidates the mechanism by which QSP delay IVDD，identifies tetrandrine as its effective component，and demonstrates that tetrandrine mitigates IVDD and NP cell senescence by regulating the PI3K/AKT signaling pathway. |
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