The protective effect and mechanism of Taraxasterol on Erastin induced ferroptosis in chondrocytes
10.19405/j.cnki.issn1000-1492.2024.06.022
- VernacularTitle:蒲公英甾醇对Erastin诱导的软骨细胞铁死亡的保护作用及机制
- Author:
Fuli ZHOU
1
,
2
;
Hao WANG
;
Rendi ZHU
;
Yingjie ZHAO
;
Yaru YANG
;
Renpeng ZHOU
;
Wei HU
;
Chao LU
Author Information
1. 安徽医科大学药学院,合肥 230032
2. 安徽医科大学第二附属医院药物临床试验研究中心,合肥 230601
- 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 chon-drocytes in vitro and the experiments were divided into Control,Erastin,TAR,and TAR+Erastin groups.Cell via-bility 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 stai-ning 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 pro-tein expression(P＜0.01)and increased GPX4 protein expression(P＜0.01).In addition,TAR restored the re-duced cell viability caused by IL-1 β 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.
