التفاصيل البيبلوغرافية
| العنوان: |
Berberine Attenuates IL-1β-Induced Damage of Nucleus Pulposus Cells via Activating the AMPK/mTOR/Ulk1 Pathway. |
| المؤلفون: |
Huang, Liaoyuan, Chen, Jianming, Wu, Danhai, Wang, Kan, Lou, Weigang, Wu, Jianmin |
| المصدر: |
BioMed Research International; 7/23/2022, p1-11, 11p |
| مصطلحات موضوعية: |
THERAPEUTIC use of alkaloids, INTERLEUKINS, SPINE diseases, STAINS & staining (Microscopy), ALKALOIDS, ANIMAL experimentation, AUTOPHAGY, INTERVERTEBRAL disk, MTOR inhibitors, SIGNAL peptides, APOPTOSIS, HEALTH outcome assessment, CELLULAR signal transduction, CELL nuclei, RATS, IMMUNOBLOTTING, CELL proliferation, FLUORESCENT antibody technique, DESCRIPTIVE statistics, PHARMACODYNAMICS |
| مستخلص: |
Intervertebral disc degeneration (IDD) is a chronic progressive condition mainly caused by excessive inflammatory cytokines. Berberine (BBR) exerts anti-inflammatory effect on diseases and protective effect against IDD. However, the mechanism is not uncertain. This study is aimed at investigating the molecular mechanism of BBR on IDD. Nucleus pulposus (NP) cells were treated with BBR at different concentrations. The IDD rat model was established by acupuncture. The effect of BBR on interleukin- (IL-) 1β-induced cell proliferation was measured by CCK-8 assay and BrdU staining. The role of BBR in IL-1β-induced apoptosis, autophagy repression, and extracellular matrix (ECM) degradation was measured by Annexin/PI staining, immunofluorescence, and immunoblot. The effect of BBR on IDD was investigated in rat. Our findings showed that BBR restored cell growth and attenuated apoptosis in IL-1β-induced NP cells. BBR also prevented the IL-1β-induced ECM degradation through regulating ECM-related enzymes and factors. Additionally, BBR significantly activated autophagy repressed by IL-1β. Autophagy stimulated by BBR was diminished by the inhibition of the AMPK/mTOR/Ulk1 signaling pathway. In vivo study also showed BBR attenuated intervertebral disc degeneration. BBR could attenuate NP cells apoptosis and ECM degradation induced by IL-1β through autophagy by the AMPK/mTOR/Ulk1 pathway. This study suggests BBR might function as an AMPK activator to alleviate IDD progression. [ABSTRACT FROM AUTHOR] |
|
Copyright of BioMed Research International is the property of Hindawi Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder