Clematichinenoside AR protects bone marrow mesenchymal stem cells from hypoxia-induced apoptosis by maintaining mitochondrial homeostasis.
10.19540/j.cnki.cjcmm.20241014.704
- Author:
Zi-Tong ZHAO
1
;
Peng-Cheng TU
2
;
Xiao-Xian SUN
3
;
Ya-Lan PAN
4
;
Yang GUO
2
;
Li-Ning WANG
1
;
Yong MA
5
Author Information
1. School of Integrative Medicine, Nanjing University of Chinese Medicine Nanjing 210023, China Laboratory of New Techniques of Restoration and Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine Nanjing 210023, China.
2. Laboratory of New Techniques of Restoration and Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine Nanjing 210023, China Affiliated Hospital of Nanjing University of Chinese Medicine Nanjing 210029, China.
3. Laboratory of New Techniques of Restoration and Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine Nanjing 210023, China Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine Wuxi 214071, China.
4. Laboratory of New Techniques of Restoration and Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine Nanjing 210023, China Institute of Integrative Medicine Nursing Research, Nanjing University of Chinese Medicine Nanjing 210029, China.
5. School of Integrative Medicine, Nanjing University of Chinese Medicine Nanjing 210023, China Laboratory of New Techniques of Restoration and Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine Nanjing 210023, China Affiliated Hospital of Nanjing University of Chinese Medicine Nanjing 210029, China.
- Publication Type:Journal Article
- Keywords:
OPA1;
apoptosis;
bone marrow mesenchymal stem cells;
clematichinenoside AR;
mitochondrial homeostasis
- MeSH:
Mesenchymal Stem Cells/metabolism*;
Apoptosis/drug effects*;
Mitochondria/metabolism*;
Animals;
Rats;
Cell Hypoxia/drug effects*;
Homeostasis/drug effects*;
Reactive Oxygen Species/metabolism*;
Rats, Sprague-Dawley;
Membrane Potential, Mitochondrial/drug effects*;
Saponins/pharmacology*;
Caspase 3/genetics*;
Male;
bcl-2-Associated X Protein/genetics*;
Bone Marrow Cells/metabolism*;
Cell Proliferation/drug effects*;
Protective Agents/pharmacology*;
Cells, Cultured
- From:
China Journal of Chinese Materia Medica
2025;50(5):1331-1339
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to elucidate the role and mechanism of clematichinenoside AR(CAR) in protecting bone marrow mesenchymal stem cells(BMSCs) from hypoxia-induced apoptosis. BMSCs were isolated by the bone fragment method and identified by flow cytometry. Cells were cultured under normal conditions(37℃, 5% CO_2) and hypoxic conditions(37℃, 90% N_2, 5% CO_2) and treated with CAR. The BMSCs were classified into eight groups: control(normal conditions), CAR(normal conditions + CAR), hypoxia 24 h, hypoxia 24 h + CAR, hypoxia 48 h, hypoxia 48 h + CAR, hypoxia 72 h, and hypoxia 72 h + CAR. The cell counting kit-8(CCK-8) assay and terminal-deoxynucleoitidyl transferase mediated nick end labeling(TUNEL) were employed to measure cell proliferation and apoptosis, respectively. The number of mitochondria and mitochondrial membrane potential were measured by MitoTracker®Red CM-H2XRo staining and JC-1 staining, respectively. The level of reactive oxygen species(ROS) was measured with the DCFH-DA fluorescence probe. The protein levels of B-cell lymphoma-2 associated X protein(BAX), caspase-3, and optic atrophy 1(OPA1) were determined by Western blot. The results demonstrated that CAR significantly increased cell proliferation. Compared with the control group, the hypoxia groups showed increased apoptosis rates, reduced mitochondria, elevated ROS levels, decreased mitochondrial membrane potential, upregulated expression of BAX and caspase-3, and downregulated expression of OPA1. In comparison to the corresponding hypoxia groups, CAR intervention significantly decreased the apoptosis rate, increased mitochondria, reduced ROS levels, elevated mitochondrial membrane potential, downregulated the expression of BAX and caspase-3, and upregulated the expression of OPA1. Therefore, it can be concluded that CAR may exert an anti-apoptotic effect on BMSCs under hypoxic conditions by regulating OPA1 to maintain mitochondrial homeostasis.
