Lutein, as an antioxidant, has multiple conjugated double bonds in its molecular structure, which can scavenge oxygen free radicals through reduction. Lutein can quench singlet oxygen, protect lipids from singlet oxygen attack, and reduce Lipid peroxide (LOP) is produced, which inhibits the activity of ROS and prevents the destruction of normal cells by ROS; in addition, the good antioxidant effect of lutein is also accomplished by reducing the expression of inflammatory factors and increasing superoxide dismutase .
Experimental studies have found that lutein can reduce the oxidative damage caused by ROS to liver cell DNA by inhibiting Fe2 + and H2O2 levels. Through the establishment of a male rat aging model, it was found that lutein can significantly reduce the content of malondialdehyde (MDA) in serum and liver homogenate, and the activities of blood SOD and GSH-Px are also significantly higher than that of the model group, indicating that lutein can enhance The antioxidant capacity of the rat's body, thereby delaying the senescence of the rat. Using a mouse model of endotoxin-induced ocular uveitis, it was found that lutein can relieve the concentration of oxidative active substances in the eyes of mice, reduce the expression of inflammatory factors, and protect the pathological changes of Muller glial cells, indicating that lutein is in the uvea It can protect the optic nerve cells through anti-oxidation during inflammation. For the rat model of ischemia-reperfusion injury, lutein treatment can also significantly reduce the oxidative pressure of bone tissue, protein carbonylation and sulfhydryl groups, and lipid peroxidation. Lutein also plays an important role in the protection of brain tissue. Studies have found that the expression of inflammatory factors IL-1β, IL-6, and serum ROS concentration in rats with severe traumatic brain injury after pretreatment with lutein is significantly reduced. Lutein can effectively protect severe traumatic brain injury by reducing inflammation and oxidation.