2. Academic Validation
  3. Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

Leonurine Protects Bone Mesenchymal Stem Cells from Oxidative Stress by Activating Mitophagy through PI3K/Akt/mTOR Pathway

  • Cells. 2022 May 24;11(11):1724. doi: 10.3390/cells11111724.
Bingkun Zhao 1 2,  Qian Peng 1,  Dan Wang 3 4,  Rong Zhou 1,  Raorao Wang 1,  Yizhun Zhu 5,  Shengcai Qi 1 6 7
Affiliations

Affiliations

  • 1 Department of Stomatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
  • 2 Department of Plastic Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221000, China.
  • 3 Institute for Tissue Engineering and Regenerative Medicine, The Chinese University of Hong Kong, Hong Kong, China.
  • 4 School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
  • 5 State Key Laboratory of Quality Research in Chinese Medicine, School of Pharmacy, Macau University of Science and Technology, Macau SAR 999078, China.
  • 6 Department of Prothodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai 200001, China.
  • 7 Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai 200001, China.
PMID: 35681421 DOI: 10.3390/cells11111724
Abstract

Osteoporosis bears an imbalance between bone formation and resorption, which is strongly related to oxidative stress. The function of leonurine on bone marrow-derived mesenchymal stem cells (BMSCs) under oxidative stress is still unclear. Therefore, this study was aimed at identifying the protective effect of leonurine on H2O2 stimulated rat BMSCs. We found that leonurine can alleviate cell Apoptosis and promote the differentiation ability of rat BMSCs induced by oxidative stress at an appropriate concentration at 10 μM. Meanwhile, the intracellular ROS level and the level of the COX2 and NOX4 mRNA decreased after leonurine treatment in vitro. The ATP level and mitochondrial membrane potential were upregulated after leonurine treatment. The protein level of PINK1 and Parkin showed the same trend. The mitophage in rat BMSCs blocked by 3-MA was partially rescued by leonurine. Bioinformatics analysis and leonurine-protein coupling provides a strong direct combination between leonurine and the PI3K protein at the position of Asp841, Glu880, Val882. In conclusion, leonurine protects the proliferation and differentiation of BMSCs from oxidative stress by activating Mitophagy, which depends on the PI3K/Akt/mTOR pathway. The results showed that leonurine may have potential usage in osteoporosis and bone defect repair in osteoporosis patients.

Keywords

leonurine; mitophagy; osteoporosis.

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