The protective effect and mechanism of Taraxasterol on Erastin induced ferroptosis in chondrocytes
10.19405/j.cnki.issn1000-1492.2024.06.022
- Author:
Fuli Zhou
1
,
2
;
Hao Wang
1
,
2
;
Rendi Zhu
1
,
2
;
Yingjie Zhao
1
,
2
;
Yaru Yang
1
,
2
;
Renpeng Zhou
1
,
2
;
Wei Hu
1
,
2
;
Chao Lu
1
,
3
Author Information
1. School of Pharmacy,Anhui Medical University,Hefei 230032
2. Dept of Clinical Pharmacology, The Second Afiliated Hospital of Anhui Medical University,Hefei 230601
3. Dept of Clinical Pharmacology, The First Afiliated Hospital ,Anhui University of Science and Technology,Huainan 232007
- Publication Type:Journal Article
- Keywords:
taraxasterol;
chondrocytes;
ferroptosis;
osteoarthritis
- From:
Acta Universitatis Medicinalis Anhui
2024;59(6):1053-1059
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the role of Taraxasterol ( TAR) on ferroptosis in chondrocytes induced by Erastin.
Methods :The C28/I2 chondrocyte line was treated with Erastin to construct the ferroptosis model of chondrocytes in vitro and the experiments were divided into Control , Erastin , TAR , and TAR + Erastin groups. Cell viability was detected by the CCK⁃8 assay. Cytotoxicity was detected by the lactate dehydrogenase (LDH) kit and the Calcein/PI cytokinesis kit. Flow cytometry was used to detect lipid reactive oxygen species (ROS) . The intracellular glutathione (GSH) content was detected by GSH kit. Mitochondrial membrane potential was detected by JC⁃1 staining and RH123 staining. ACSL4 and GPX4 protein expression and the key indicators of ferroptosis were detected by Western blot.
Results :TAR restored the decreased cell viability of C28/I2 chondrocytes induced by Erastin treatment as well as reduced Erastin⁃induced cytotoxicity (P < 0. 01) . Compared with the control group , the level of
intracellular lipid ROS increased( P < 0. 01) and the content of GSH decreased( P < 0. 01) after treatment with Erastin ,while TAR could reduce the production of lipid ROS ( P < 0. 01) and increase the content of GSH ( P < 0. 01) . TAR restored mitochondrial membrane potential in C28/I2 chondrocytes ferroptosis , decreased ACSL4 protein expression (P < 0. 01) and increased GPX4 protein expression (P < 0. 01) . In addition , TAR restored the reduced cell viability caused by IL⁃1β treatment.
Conclusion :TAR can inhibit Erastin induced ferroptosis in C28/I2 chondrocytes ,which may be related to the regulation of ACSL4 and GPX4 protein expression.
- Full text:2024082011472256281蒲公英甾醇对Erastin...细胞铁死亡的保护作用及机制_周富丽.pdf
