iPLA2 β prevents high glucose －induced injury of human renal tubular epithelial cells via regulating ferroptosis
10.19405/j.cnki.issn1000-1492.2023.03.006
- Author:
Lu Xue
1
;
Jingjing Wang
2
;
Xueru Hu
2
;
Yonggui Wu
2
;
Xiangming Qi
3
,
4
Author Information
1. Dept of Nephrology，Fuyang Hospital Affiliated to Anhui Medical University，Fuyang 236000
2. Dept of Nephrology，The First Affiliated Hospital of Anhui Medical University，Hefei 230022
3. Dept of Nephrology，Fuyang Hospital Affiliated to Anhui Medical University，Fuyang 236000
4. Dept of Nephrology，The First Affiliated Hospital of Anhui Medical University，Hefei 230022
- Publication Type:Journal Article
- Keywords:
human renal tubular epithelial cells;
diabetic kidney disease;
ferroptosis;
iPLA2 β
- From:
Acta Universitatis Medicinalis Anhui
2023;58(3):379-385
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the expression of Ca2 + -independent phospholipase A2 β (iPLA2 β) in human renal tubular epithelial cells (HK-2) induced by high glucose(HG) ，the relationship between iPLA2 β and ferroptosis and the protective mechanism of HG treated HK-2 cells．
Methods:The HK-2 cells were treated with 30 mmol /L glucose，the overexpression model was constructed by transfection of iPLA2 β plasmid．Ferrostatin-1 ( Fer1) (an inhibitor of ferroptosis) and erastin (an activator of ferroptosis) were used as controls．After 36 hours of intervention，the kit detected the levels of superoxide (SOD) ，malonaldehyde(MDA) and iron in HK-2 cells．DCF immunofluorescence was used to detect intracellular reactive oxygen species ( ROS) ．The expression of ACSL4， GPX4，LPCAT3，TFR1 in HK-2 cells were measured by Western blot.
Results :The expression of iPLA2 β downregulated in HG-induced injury of HK-2 cells．The levels of ROS and MDA in HK-2 cells increased，while the levels of GSH and SOD decreased．The expression of ACSL4，LPCAT3 and TFR1 decreased，and the expression of GPX4 increased in HK-2 cells．However，these indexes were improved after Fer-1 intervention．iPLA2 β overexpression could reduce the injury of HK-2 cells via attenuation of KIM-1． Further research revealed that iPLA2 β overexpression inhibited oxidative stress and ferroptosis in HK-2 cells injury induced by high glucose．Meanwhile，
the improvement effect of iPLA2 β on HG-induced HK-2 cells damage could be eliminated by erastin．
Conclusion:iPLA2 β prevents HG-induced injury of HK-2 cells via regulating ferroptosis.
- Full text:2024071611324934721iPLA2β通过调控铁死亡...诱导的人肾小管上皮细胞损伤_薛璐.pdf
