Epigallocatechin-3-gallate attenuates microcystin-LR induced oxidative stress and inflammation in human umbilical vein endothelial cells

• Published in: Chemosphere (Oxford) 2017-02, Vol.168, p.25-31
• Main Authors: Shi, Jun, Deng, Huiping, Pan, Huichao, Xu, Yinjie, Zhang, Min
• Format: Article
• Language: English
• Subjects: Angiogenesis; Anti-Inflammatory Agents - pharmacology; Antioxidants - pharmacology; Catechin - analogs & derivatives; Catechin - pharmacology; Epigallocatechin-3-gallate; Human Umbilical Vein Endothelial Cells; Humans; Inflammation - chemically induced; Inflammation - drug therapy; Interleukin-6 - metabolism; Microcystin-LR; Microcystins - drug effects; NF-kappa B p50 Subunit - metabolism; Reactive oxygen species; Reactive Oxygen Species - metabolism; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2016.10.037

Epigallocatechin-3-gallate (EGCG) has been shown to possess anti-inflammatory effects. Microcystin-LR (MC-LR) is a potent toxin and our past research suggested that it also mediated human umbilical vein endothelial cell (HUVEC) injury. The aim of this study was to investigate the effects of EGCG on MC-LR-induced oxidative stress and inflammatory responses in HUVECs. HUVECs were stimulated with MC-LR in the presence or absence of EGCG. MC-LR (40 μM) significantly increased cell death and decreased cell viability, migration, and tube formation, whereas EGCG (50 μM) inhibited these effects. Furthermore, the results indicated that EGCG inhibited the production of reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) in MC-LR-stimulated HUVECs. Compared with MC-LR, EGCG significantly increased superoxide dismutase (SOD) and glutathione (GSH) levels and decreased malondialdehyde (MDA) levels. Moreover, the analysis indicated that EGCG suppressed MC-LR-induced NF-κB activation. In conclusion, the effects of EGCG were associated with inhibition of the NF-κB signaling pathway, which resulted in decreased ROS and TNF-α, thereby attenuating MC-LR-mediated oxidative and inflammatory responses. •EGCG effect on MC-LR-induced oxidative and inflammatory responses was evaluated.•EGCG inhibited MC-LR-induced HUVEC death.•EGCG inhibited MC-LR-induced decrease in HUVEC viability and migration.•EGCG attenuated MC-LR-mediated oxidative and inflammatory responses.•EGCG decreased inflammation by suppressing MC-LR-induced NF-κB activation.