Oral Administration of Lutein Improves Fat Graft Survival by Alleviating Oxidative Stress in Mice

Oxidative stress induced by ischemia and hypoxia in fat transplantation is a major obstacle to graft retention. Previous studies have shown that lutein has excellent adipose tissue affinity and antioxidative stress ability, however, the effects of oral lutein on fat transplantation have not yet been studied.

We aimed to investigate whether oral lutein could improve fat transplantation retention by regulating oxidative stress, apoptosis, and inflammatory cytokine levels in graft tissues.

Nude mice were assigned to the control group (normal saline), low-dose lutein group (10 mg/kg/day), and high-dose lutein group (20 mg/kg/day) randomly. All mice received treatment by gavage 1 week before fat grafting and continued for 2 weeks. The grafts were collected 1, 2, and 12 weeks after treatment. By conducting histological analyses, Western blotting, quantitative polymerase chain reaction and cell metabolic function detection, the regulatory effects of lutein on apoptosis and oxidative stress in grafts were demonstrated. Additionally, RNA sequencing was conducted to further clarify the efficacy of lutein on fat grafting.

Lutein induced superior graft retention, histological structures, and more viable adipocytes than the control group. It relieved tissue oxidative stress and lipid oxidative damage by decreasing reactive oxygen species and significantly reduced inflammation and apoptosis of grafts. RNA sequencing analysis confirmed that lutein could downregulate the gene expression of oxidative stress and related inflammation and apoptosis.

Our study suggests that oral administration of lutein can improve fat graft survival by reducing the levels of oxidative stress, inflammation, and apoptosis in grafted fat.