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Updated: Jan 23, 2026

Isolation, Culture, and Differentiation of Bone Marrow Stromal Cells and Osteoclast Progenitors from Mice
Published on: January 6, 2018
[Oxidative Damage of Bone Marrow Stromal Cells Caused by Chemotherapy Drugs]
Zhe Liu1, Yi-Hui Li1, Zhen-Ya Xue1
1State Key Laboratory of Experimental Hematology,Institute of Hematology &Blood Diseases Hospital,Chinese Academy of Medical Sciences & Peking Union Medical College,Tianjin 300020,China.
Objective:
To explore the oxidative damage of OP9 cells induced by daunorubicin (DNR) treatment.
Methods:
The TMRM probe was used to detect mitochondrial membrane potential by flow cytometry; the reactive oxygen species (ROS) was determined by flow cytometry DCFDA probe; the real-time PCR was used to detect the molecular expression of antioxidant enzyme,glutathione peroxidase (GPX) in OP9 cells; the expression of γ-H2AX was determined by flow cytometry.
Results:
Compared with normal OP9 cells, the positive rate of TMRM in DNR-treated OP9 cells decreased by 56.7% (P<0.05); the positive rate of DCFDA in DNR-treated OP9 cells increased by 3.52 times (P<0.01). Compared with normal OP9 cells, DNR-treated OP9 cells showed a decrease in the expression of GPX4 by 44.22% (P<0.001); the expression of GPX7 decreased by 65.7% (P<0.001); the expression of GPX8 decreased by 24.7% (P<0.001); the positive rate of γ-H2AX in DNR-treated OP9 cells increased (P<0.05).
Conclusion:
After DNR treatment, mitochondrial membrane potential of OP9 cells decreases; the level of reactive oxygen species increases; the expression of glutathione peroxidase (GPX) molecules decreases significantly; genomic instability increases obviously; the oxidative damage of cells increased.
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