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- Title
4- 羟基过氧环磷酰胺通过靶向P53损伤人卵巢颗粒细胞线粒体 自噬功能的研究.
- Authors
赵辰希; 徐 聪; 谢思远; 高 超; 覃莲菊; 吴 畏
- Abstract
Objective: To investigate the effect of the in vitro activation product of cyclophosphamide, 4 - hydroperoxy cyclophosphamide (4-HC), on the functional impairment of the human ovarian granulosa cell line SVOG, and the potential underlying mechanisms. Methods: SVOG cells were treated with 0.2, 2.0, and 10.0 μmol/L of 4-HC for 24, 48, and 72 h. The cell viability in each group was measured using the CCK-8 assay to determine the optimal time and concentration for constructing an injury model. Western blot and RT -qPCR were used to detect changes in mitochondrial autophagy flux. Transmission electron microscopy was employed to observe mitochondrial changes in both normal and 4-HC -injured cells. RT -qPCR was used to assess the expression of P53- related genes, and immunofluorescence was applied to detect the expression levels of P53, Parkin, and the translocase of the outer mitochondrial membrane 20 (TOMM20) proteins. Results: A model of SVOG cell injury induced by 2.0 μmol/L 4-HC for 48 h was established in vitro. Mitochondrial autophagy flux was inhibited, and mitochondrial morphology was abnormal in 4-HC-injured SVOG cells, with a significant increase in damaged mitochondria. The expression level of P53 was significantly increased in 4-HC -injured SVOG cells. An increase in the cytoplasmic interaction between P53 and Parkin protein was observed, while the binding of TOMM20 and Parkin protein was inhibited in 4 - HC -injured SVOG cells. Conclusion: In vitro, 4 - HC may induce damage to human ovarian granulosa cells by inhibiting mitochondrial autophagy through the P53-Parkin pathway.
- Subjects
PARKIN (Protein); GRANULOSA cells; CELL survival; TRANSMISSION electron microscopy; P53 protein; AUTOPHAGY
- Publication
Journal of Nanjing Medical University: Natural Sciences, 2024, Vol 44, Issue 12, p1629
- ISSN
1007-4368
- Publication type
Academic Journal
- DOI
10.7655/NYDXBNSN240993