Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats
Apoptosis and extracellular matrix degradation of the nucleus pulposus are the main initiators of intervertebral disc degeneration (IVDD) and can be explained by endoplasmic reticulum (ER) stress. Thus, pharmacological therapy aimed at suppressing this pathway may be a promising approach for the man...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2023-01-01
|
| Series: | Frontiers in Pharmacology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2023.1095307/full |
| _version_ | 1797947085497040896 |
|---|---|
| author | Yan Chen Yan Chen Baixing Li Baixing Li Yue Xu Tangjun Zhou Tangjun Zhou Changqing Zhao Changqing Zhao Jie Zhao Jie Zhao |
| author_facet | Yan Chen Yan Chen Baixing Li Baixing Li Yue Xu Tangjun Zhou Tangjun Zhou Changqing Zhao Changqing Zhao Jie Zhao Jie Zhao |
| author_sort | Yan Chen |
| collection | DOAJ |
| description | Apoptosis and extracellular matrix degradation of the nucleus pulposus are the main initiators of intervertebral disc degeneration (IVDD) and can be explained by endoplasmic reticulum (ER) stress. Thus, pharmacological therapy aimed at suppressing this pathway may be a promising approach for the management of intervertebral disc degeneration. In this study, we aimed to explore the protective effects of Sal003 against intervertebral disc degeneration and its underlying mechanisms. Thapsigargin (Tg)-stimulated rat nucleus pulposus cells and a needle puncture-induced intervertebral disc degeneration rat model were used to explore the protective effects of Sal003. Our results showed that Sal003 inhibited apoptosis and extracellular matrix degradation by suppressing the endoplasmic reticulum stress pathway. The therapeutic effects of Sal003 were also observed in the intervertebral disc degeneration rat model, as evidenced by improved degeneration along with decreased apoptosis and extracellular matrix degradation in intervertebral discs. Our results demonstrated Sal003 as a potential treatment for intervertebral disc degeneration. |
| first_indexed | 2024-04-10T21:21:11Z |
| format | Article |
| id | doaj.art-db1eca9175b049a0b3604404404a8601 |
| institution | Directory Open Access Journal |
| issn | 1663-9812 |
| language | English |
| last_indexed | 2024-04-10T21:21:11Z |
| publishDate | 2023-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pharmacology |
| spelling | doaj.art-db1eca9175b049a0b3604404404a86012023-01-20T04:58:11ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122023-01-011410.3389/fphar.2023.10953071095307Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in ratsYan Chen0Yan Chen1Baixing Li2Baixing Li3Yue Xu4Tangjun Zhou5Tangjun Zhou6Changqing Zhao7Changqing Zhao8Jie Zhao9Jie Zhao10Department of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaChangshu Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, Jiangsu, ChinaDepartment of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaApoptosis and extracellular matrix degradation of the nucleus pulposus are the main initiators of intervertebral disc degeneration (IVDD) and can be explained by endoplasmic reticulum (ER) stress. Thus, pharmacological therapy aimed at suppressing this pathway may be a promising approach for the management of intervertebral disc degeneration. In this study, we aimed to explore the protective effects of Sal003 against intervertebral disc degeneration and its underlying mechanisms. Thapsigargin (Tg)-stimulated rat nucleus pulposus cells and a needle puncture-induced intervertebral disc degeneration rat model were used to explore the protective effects of Sal003. Our results showed that Sal003 inhibited apoptosis and extracellular matrix degradation by suppressing the endoplasmic reticulum stress pathway. The therapeutic effects of Sal003 were also observed in the intervertebral disc degeneration rat model, as evidenced by improved degeneration along with decreased apoptosis and extracellular matrix degradation in intervertebral discs. Our results demonstrated Sal003 as a potential treatment for intervertebral disc degeneration.https://www.frontiersin.org/articles/10.3389/fphar.2023.1095307/fullER stress pathwaySal003intervertebral disc degenerationapoptosisextracellular matrix degradation |
| spellingShingle | Yan Chen Yan Chen Baixing Li Baixing Li Yue Xu Tangjun Zhou Tangjun Zhou Changqing Zhao Changqing Zhao Jie Zhao Jie Zhao Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats Frontiers in Pharmacology ER stress pathway Sal003 intervertebral disc degeneration apoptosis extracellular matrix degradation |
| title | Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| title_full | Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| title_fullStr | Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| title_full_unstemmed | Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| title_short | Sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| title_sort | sal003 alleviated intervertebral disc degeneration by inhibiting apoptosis and extracellular matrix degradation through suppressing endoplasmic reticulum stress pathway in rats |
| topic | ER stress pathway Sal003 intervertebral disc degeneration apoptosis extracellular matrix degradation |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2023.1095307/full |
| work_keys_str_mv | AT yanchen sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT yanchen sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT baixingli sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT baixingli sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT yuexu sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT tangjunzhou sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT tangjunzhou sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT changqingzhao sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT changqingzhao sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT jiezhao sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats AT jiezhao sal003alleviatedintervertebraldiscdegenerationbyinhibitingapoptosisandextracellularmatrixdegradationthroughsuppressingendoplasmicreticulumstresspathwayinrats |