Biophotin attenuates hypoxia/reoxygenation-induced endothelial cell injury by inhibiting inflammation

AIM  To study the protective effects and mechanisms of biophotin on hypoxia/reoxygenation (H/R)-induced endothelial cell injury.

METHODS  Endothelial cells of mouse coronary arteries were divided into control, H/R and H/R+biophotin groups after H/R-induced endothelial cell injury. The viability of endothelial cells was analyzed by CCK-8, the migration rate of endothelial cells was determined by cell scratch assay, the apoptosis and positive expression of cells were detected by flow cytometry, and the NO secretion of endothelial cells was determined by NO kit. eNOS, VEGF and TNF-α were detected by real-time polymerase chain reaction (RT-PCR). Real-time polymerase chain reaction (RT-PCR) was used to measure the mRNA levels of inflammatory factors such as eNOS, VEGF and TNF-α, and ELISA kits were used to measure the levels of TNF-α and IL-1β in macrophages.

RESULTS  Compared with those in the control group, endothelial cell activity was weakened in the H/R group (P<0.01), NO release, cell migration, eNOS and VEGF mRNA levels were reduced (P<0.05), and apoptosis and mRNA levels of inflammatory factors, such as TNF-α, were increased (P<0.05, P<0.01). Compared with those in the H/R group, endothelial cells in the H/R+ group showed higher levels of inflammatory factors, such as TNF-α and IL-1β, in the biophotin group (P<0.05, P<0.01). Compared with those in the H/R group, the activity of endothelial cells in the H/R+ group was enhanced (P<0.01), NO release and cell migration, eNOS and VEGF mRNA levels were increased (P<0.05, P<0.01), and apoptosis and mRNA levels of inflammatory factors, such as TNF-α, were decreased (P<0.05, P<0.01).

CONCLUSION  Biophotin has a protective effect against H/R-induced endothelial cell injury and improves cardiovascular diseases caused by endothelial injury.