Abstract | BACKGROUND: METHODS:
Interleukin (IL)-1β (10 ng/ml) was adopted to induce human nucleus pulposus cells (HNPCs) as a cell model for IDD. The effects of different concentrations of ATG (0, 2, 5, 10, 20, 50 μmol/L) on the viability of HNPCs and effects of ATG (10, 50 μmol/L) on the viability of IL-1β-induced HNPCs were detected by cell counting kit-8 (CCK-8). After IL-1β-induced HNPCs were transfected with miR-483-3p inhibitor and/or treated with ATG, cell viability and apoptosis were determined by CCK-8 and flow cytometry; the expressions of miR-483-3p, extracellular matrix (ECM)-related genes, and inflammation-related genes were measured by quantitative real time polymerase chain reaction (qRT-PCR), and expressions of ECM/apoptosis/NF-κB pathway-related proteins were quantified by Western blot. RESULTS: ATG had no significant effect on the viability of HNPCs but could promote the viability of IL-1β-induced HNPCs. ATG inhibited apoptosis, ECM degradation, inflammation, and activation of NF-κB pathway in HNPCs induced by IL-1β, but promoted the expression of miR-483-3p. MiR-483-3p inhibitor reversed the above-mentioned regulatory effects of ATG. CONCLUSION:
Arctigenin suppresses apoptosis, ECM degradation, inflammation, and NF-κB pathway activation in HNPCs by up-regulating miR-483-3p.
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Authors | Zhe Ji, Rui Guo, Zhigang Ma, Hongwei Li |
Journal | Journal of clinical laboratory analysis
(J Clin Lab Anal)
Vol. 36
Issue 7
Pg. e24508
(Jul 2022)
ISSN: 1098-2825 [Electronic] United States |
PMID | 35689566
(Publication Type: Journal Article)
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Copyright | © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. |
Chemical References |
- Extracellular Matrix Proteins
- Furans
- Lignans
- MIRN483 microRNA, human
- MicroRNAs
- NF-kappa B
- arctigenin
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Topics |
- Apoptosis
(genetics)
- Cells, Cultured
- Extracellular Matrix
(metabolism)
- Extracellular Matrix Proteins
(genetics)
- Furans
(pharmacology)
- Humans
- Inflammation
(genetics, metabolism)
- Intervertebral Disc Degeneration
(drug therapy, genetics)
- Lignans
(pharmacology)
- MicroRNAs
(genetics, metabolism)
- NF-kappa B
(genetics, metabolism)
- Nucleus Pulposus
(metabolism)
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