Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration

Abstract Objective To explore the potential mechanism of Yougui Wan on deformed lumbar intervertebral disk structure in rats. Methods Thirty male Sprague–Dawley rats were randomly divided into 3 groups, with 10 rats in each group. The animals in the blank control group were healthy rats without spec...

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Main Authors: She Ma, Kan Liu, Jing-yan Yang, Ren-jun Huang, Dong Yu
Format: Article
Language:English
Published: BMC 2024-01-01
Series:Journal of Orthopaedic Surgery and Research
Subjects:
Online Access:https://doi.org/10.1186/s13018-024-04554-w
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author She Ma
Kan Liu
Jing-yan Yang
Ren-jun Huang
Dong Yu
author_facet She Ma
Kan Liu
Jing-yan Yang
Ren-jun Huang
Dong Yu
author_sort She Ma
collection DOAJ
description Abstract Objective To explore the potential mechanism of Yougui Wan on deformed lumbar intervertebral disk structure in rats. Methods Thirty male Sprague–Dawley rats were randomly divided into 3 groups, with 10 rats in each group. The animals in the blank control group were healthy rats without specific treatment, and those in the model group and traditional Chinese medicine (TCM) group were used to establish the intervertebral disk degeneration (IDD) model by puncturing the annulus. Four weeks after modeling, rats in the TCM group were administered Yougui Wan by gavage for 2 consecutive weeks. Serum interleukin-6 (IL-10), macrophage migration inhibitory factor (MIF) and tumor necrosis factor alpha (TNF-α) levels were measured by ELISA, and the protein expression levels of collagen II and Notch1 in intervertebral disk tissues were examined by Western blotting. Apoptosis was detected by the TUNEL method. Results Compared with those in the blank group, IL-10, MIF and TNF-α levels in the model group and TCM group were increased (P < 0.05), the protein expression levels of collagen II were decreased, and the protein expression levels of Notch1 were increased. Compared with those in the model group, the levels of IL-10 in the TCM group were increased (P < 0.05), the levels of MIF and TNF-α were decreased (P < 0.05), the protein expression levels of collagen II were increased, and the protein expression levels of Notch1 were decreased. Conclusion Yougui Wan can inhibit the inflammatory response in IDD rats, reduce the degradation of extracellular matrix, reduce apoptosis in nucleus pulposus cells, and alleviate intervertebral disk degeneration. The mechanism may be related to the regulation of the Notch signaling pathway.
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spelling doaj.art-10c7c50457da44e9b88f652dade469572024-03-05T16:36:21ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2024-01-011911610.1186/s13018-024-04554-wTherapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degenerationShe Ma0Kan Liu1Jing-yan Yang2Ren-jun Huang3Dong Yu4Beijing University of Chinese MedicineDepartment of Orthopedics, Beijing University of Chinese Medicine Third Affiliated HospitalBeijing University of Chinese MedicineBeijing University of Chinese MedicineDepartment of Orthopedics, Beijing University of Chinese Medicine Third Affiliated HospitalAbstract Objective To explore the potential mechanism of Yougui Wan on deformed lumbar intervertebral disk structure in rats. Methods Thirty male Sprague–Dawley rats were randomly divided into 3 groups, with 10 rats in each group. The animals in the blank control group were healthy rats without specific treatment, and those in the model group and traditional Chinese medicine (TCM) group were used to establish the intervertebral disk degeneration (IDD) model by puncturing the annulus. Four weeks after modeling, rats in the TCM group were administered Yougui Wan by gavage for 2 consecutive weeks. Serum interleukin-6 (IL-10), macrophage migration inhibitory factor (MIF) and tumor necrosis factor alpha (TNF-α) levels were measured by ELISA, and the protein expression levels of collagen II and Notch1 in intervertebral disk tissues were examined by Western blotting. Apoptosis was detected by the TUNEL method. Results Compared with those in the blank group, IL-10, MIF and TNF-α levels in the model group and TCM group were increased (P < 0.05), the protein expression levels of collagen II were decreased, and the protein expression levels of Notch1 were increased. Compared with those in the model group, the levels of IL-10 in the TCM group were increased (P < 0.05), the levels of MIF and TNF-α were decreased (P < 0.05), the protein expression levels of collagen II were increased, and the protein expression levels of Notch1 were decreased. Conclusion Yougui Wan can inhibit the inflammatory response in IDD rats, reduce the degradation of extracellular matrix, reduce apoptosis in nucleus pulposus cells, and alleviate intervertebral disk degeneration. The mechanism may be related to the regulation of the Notch signaling pathway.https://doi.org/10.1186/s13018-024-04554-wIntervertebral disk degenerationYougui WanNotch signaling pathwayInflammatory responseNucleus pulposus cells
spellingShingle She Ma
Kan Liu
Jing-yan Yang
Ren-jun Huang
Dong Yu
Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
Journal of Orthopaedic Surgery and Research
Intervertebral disk degeneration
Yougui Wan
Notch signaling pathway
Inflammatory response
Nucleus pulposus cells
title Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
title_full Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
title_fullStr Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
title_full_unstemmed Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
title_short Therapeutic effect and mechanism of Yougui Wan in rats with intervertebral disk degeneration
title_sort therapeutic effect and mechanism of yougui wan in rats with intervertebral disk degeneration
topic Intervertebral disk degeneration
Yougui Wan
Notch signaling pathway
Inflammatory response
Nucleus pulposus cells
url https://doi.org/10.1186/s13018-024-04554-w
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