Mono-carbonyl analogues of curcumin prevents paraquat-induced apoptosis in HK-2 cell line by inhibiting oxidative damage and inflammation
10.3760/cma.j.issn.1001-9391.2017.09.001
- VernacularTitle: 单羰基姜黄素类似物对百草枯诱导HK-2细胞损伤的保护
- Author:
Guangliang HONG
1
;
Zhening YANG
;
Yiyue HE
;
Jiaping TAN
;
Guang LIANGM
;
Guangju ZHAO
;
Zhongqiu LU
Author Information
1. Emergency Department of the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
- Publication Type:Journal Article
- Keywords:
Curcumin;
Mono-carbonyl analogues of curcumin;
Paraquat;
Epithelial cell
- From:
Chinese Journal of Industrial Hygiene and Occupational Diseases
2017;35(9):641-647
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of mono-carbonyl analogues of curcumin (L6H21) on paraquat (PQ) -induced injury in HK-2 cell line and explore its underlying mechanisms.
Methods:Cultured HK-2 cells were challenged by PQ with or without L6H21 treatment. Cell viability and apoptosis were determined by CCK-8 assay and flow cytometry, respectively. Gene expressions and protein levels of apoptotic and inflammatory factors were assessed by RT-PCR, ELISA, and western blot. Intracellular ROS production was detected by DCFH-DA staining. Superoxide dismutase (SOD) and malondialdehyde (MDA) were examined by chemical colorimetry.
Results:1) PQ challenge significantly inhibited HK-2 cells proliferation, which was prevented by L6H21 administration. PQ dramatically induced HK-2 apoptosis evidenced by increasing expressions of caspase-9, caspase-3 and Bax, while decreasing Bcl-2 level. However, PQ induced these apoptotic effects in HK-2 cells were reversed by L6H21. Similarly, PQ exposure obviously enhanced activity of NF-κB and levels of cytokines (TNF-α、IL-6) in HK-2 cells, which was inhibited by L6H21. Furthermore, administration of L6H21 inhibited PQ induced ROS and MDA production, and promoted SOD level in HK-2 cells.
Conclusion:L6H21 administration inhibits PQ-induced apoptosis in HK-2 cells possibly by reducing inflammation and oxidative damage.
