CCCong Chen

Cong Chen

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Cong Chen has a total of 8 co-authors. Here are the top co-authors by number of shared publications:

  • Chengwei Liang

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication
  • Dong Zhang

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication
  • Fengjian Yang

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication
  • Jianyong Feng

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication
  • Weilong Lin

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication
  • Xuelin Zhang

    Department of Orthopaedics, Hua Dong Hospital Affiliated to Fudan University, Shanghai, China

    1 shared publication

Latest Publications

  • Naringin rescued the TNF-α-induced inhibition of osteogenesis of bone marrow-derived mesenchymal stem cells by depressing the activation of NF-кB signaling pathway

    by Xvhai Cao, Weilong Lin, Chengwei Liang, Dong Zhang, Fengjian Yang, Yan Zhang, Xuelin Zhang, Jianyong Feng, Cong Chen

    Naringin exhibits antiinflammatory activity and is shown to induce bone formation. Yet the impact of naringin on inflammation-affected bone marrow-derived mesenchymal stem cell (BM-MSC), a promising tool for the regenerative treatment of bone injury, remained to be investigated. We first cultured and characterized the BM-MSCs in vitro and observe the effects of treatments of TNF-α, naringin, or the combination of both on osteogenic differentiation. TNF-α administered at the concentration of 20 ng/ml results in significant reductions in MSC’s cell survival, alkaline phosphatase activity and expressions of two osteogenic genes, Runx2 and Osx. Simultaneous treatment of both TNF-α and naringin is able to rescue such reductions. Further mechanistic studies indicate that TNF-α treatment activates the NF-кB signaling pathway, evidenced by elevated p-IкBα level as well as the increased nuclear fraction of NF-кB subunit, p65. Finally, treatment with both TNF-α and naringin decreases expressions of p-IкBα and nuclear p65, and thus represses NF-кB pathway activated by sole TNF-α treatment. Our findings provide a molecular basis by which naringin restores the TNF-α-induced damage in MSCs and provide novel insights into the application of naringin in the MSC-based treatments for inflammation-induced bone injury.