Theaflavins prevent cartilage degeneration via AKT/FOXO3 signaling in vitro

Li,Jun; Zheng,Jianping

doi:10.3892/mmr.2018.9745

Theaflavins prevent cartilage degeneration via AKT/FOXO3 signaling in vitro

Authors:
- Jun Li
- Jianping Zheng
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Affiliations: Department of Orthopedics, Xiangyang Central Hospital, The Affiliated Hospital of Hubei College of Arts and Science, Xiangyang, Hubei 441021, P.R. China
Published online on: December 12, 2018 https://doi.org/10.3892/mmr.2018.9745
Pages: 821-830
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Theaflavins (TFs) are the main bioactive polyphenols in tea and contribute to protection against oxidative stress. Excessive reactive oxygen species (ROS) accumulation can lead to the disruption of cartilage homeostasis. The present study examined the potential effects of TFs on H2O2‑induced cartilage degeneration in vitro. Cell Counting kit (CCK‑8) was used to determine cell viability, and flow cytometric analysis was used to detect ROS, apoptosis and DNA damage. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting were used to detect the expression levels of target factors. The present study revealed that TFs effectively reduced the expression of catabolic factors, including matrix metalloproteinase‑13, interleukin‑1 and cartilage glycoprotein 39. TFs inhibited ROS generation in cartilage degeneration, and suppressed apoptosis and DNA damage caused by oxidative stress. TFs also downregulated the expression levels of cleaved caspase‑3 and B‑cell lymphoma 2‑associated X protein, and the DNA damage‑related genes, ATR serine/threonine kinase and ATM serine/threonine kinase. Furthermore, TFs enhanced the activity of glutathione peroxidase 1 and catalase, but reduced the expression levels of phosphorylated (p)‑AKT serine/threonine kinase (AKT) and p‑Forkhead box O3 (FOXO3)a. Conversely, the effects of TFs on apoptosis and DNA damage were reversed by persistent activation of AKT. In conclusion, TFs prevented cartilage degeneration via AKT/FOXO3 signaling in vitro. The present study suggested that TFs may be a potential candidate drug for the prevention of cartilage degeneration.

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