C-phycocyanin (C-PC) is an effective
antioxidant and has an important value in medical research. Oxidative stress is considered to be one of the main underlying mechanisms of cell death, and reducing oxidative stress is one of the strategies to enhance germ cell viability. Herein, we investigated the protective effect and the mechanism of C-PC and apo-
phycocyanin subunit on oxidative stress damage induced by H2 O2 in
GC-1 spg cells. C-PC genes were cloned into the pGEX-4T-1 vectorand transformed into Escherichia coli BL21 to achieve the efficient expression of C-PC subunit.
GC-1 spg cells were treated with 600 μM H2 O2 for 24 h to establish the oxidative stress damage model. Cell viability was detected by
CCK-8. The degree of oxidative stress was detected by testing
Superoxide dismutase (SOD) and
glutathione peroxidase (GPx) activities and
glutathione (GSH) and
Malondialdehyde (MDA) levels.
Reactive oxygen species (ROS) was evaluated utilizingby 2', 7'-dichlorofluorescent-diacetate (
DCFH-DA). Mitochondrial membrane potential was determined by
JC-1. Cell
necrosis rate was detected by
Annexin V-FITC/PI. Expression of
protein was detected by western blot. We found that C-PC and GST-
CPC β significantly inhibited H2 O2 -induced oxidative damage of
GC-1 spg cells, improved the ability of antioxidation, reduced ROS overproduction, and mitochondrial membrane potential loss, and inhibited the RIP-1/RIP-3/ p-MLKL signaling pathway to reduce the
necrosis rate. The results demonstrated that C-PC played a protective role against H2 O2 -induced cell damage, especially its β subunit. This study provides a theoretical basis for C-PC as a potential
protective agent of reproductive system.