p‑Coumaric acid suppresses reactive oxygen species‑induced senescence in nucleus pulposus cells
- Kunkun Sheng
- Yan Li
- Zhan Wang
- Kai Hang
- Zhaoming Ye
Affiliations: Department of Orthopedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China, Orthopedics Research Institute of Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China
- Published online on: December 30, 2021 https://doi.org/10.3892/etm.2021.11106
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p‑Coumaric acid (PCA) is a phenolic acid that is widely present in numerous plants and human diets. Studies have demonstrated the antioxidant and anti‑senescence effects of PCA in different cell types. However, the anti‑senescence effects of PCA in nucleus pulposus (NP) cells have remained to be determined. In the present study, reverse transcription‑quantitative PCR was used to measure the gene expression of Cyclooxygenase‑2 (Cox‑2), inducible nitric oxide synthase (iNOS), p53, p16, aggrecan and collagen‑2 in NP cells. Immunofluorescence staining was used to evaluate the protein expression of p53, p16 and collagen‑2 in NP cells. In addition, cell cycle of NP cells was measured by flow cytometry. β‑galactosidase staining were used to investigate the senescence of NP cells. Preliminary results indicated that PCA suppressed ROS‑induced senescence in NP cells via both the p16 and p53 pathways. NP cells were pretreated with PCA at a concentration of 10 or 50 µg/ml prior to stimulation with 200 µM hydrogen peroxide (H2O2). Pretreatment with PCA significantly inhibited H2O2‑induced cell cycle arrest in a dose‑dependent manner. PCA also reduced the gene expression of Cox‑2, iNOS, p53 and p16 induced by H2O2. By contrast, aggrecan and collagen‑2 expression in NP cells was upregulated after PCA treatment. Furthermore, PCA suppressed H2O2‑induced changes in the protein expression of p16, p53 and collagen‑2. H2O2 stimulation of NP cells increased senescence‑associated β‑galactosidase (SA‑β‑gal) activities, while PCA treatment markedly reversed these SA‑β‑gal activities. Collectively, the present results indicated that PCA attenuated H2O2‑induced oxidative stress and cellular senescence, suggesting a potential therapeutic utility of PCA in intervertebral disc degeneration.