Lutein derived fragments exhibit higher antioxidant and anti-inflammatory properties than lutein in lipopolysaccharide induced inflammation in rats

In the present study, we appraise the anti-inflammatory efficacy of lutein oxidative degradation derivatives
mediated through UV-irradiation over lutein in counteracting the inflammation induced by lipopolysaccharide
(LPS) in rats (n = 5 per group). UV-irradiated lutein fragments were identified as anhydrolutein
(B, C40H54O), 2,6,6-trimethylcyclohexa-1,4-dienylium (M1, C9H13), (2E,4E,6E,8E)-9-(4-hydroxy-2,6,6-
trimethylcyclohex-1-1en-1-yl)-3,7-dimethylnona-2,4,6,8-tetraen-1-ylium (M2, C20H29O), 4-[(1E,3E,5E,7E)-
3,7,-dimethyldeca-1,3,5,7-tetraen-1-yl]-3,5,5-methylcyclohex-3-en-1-ol (M3, C21H30O) and zeaxanthin
(M4, C40H56O) and its isomers as 13’-Z zeaxanthin, 13’-Z lutein, all-trans zeaxanthin, and 9-Z lutein.
Induction of inflammation by LPS significantly increased the production of nitrites (3.3 fold in the serum
and 2.6 fold in the liver), prostaglandin E2 (26 fold in the serum), and pro-inflammatory cytokines like
tumor necrosis factor-α (6.6 fold in the serum), and interleukin-6 (4.8 fold in the serum). Oxidative derivatives
of lutein, especially M1, M2 and M3, ameliorated acute inflammation in rats by inhibiting the production
of nitrites, malondialdehyde (MDA), PGE2, TNF-α, and IL-6 cytokines more efficiently than lutein
in rats. The anti-inflammatory mechanism of derivatives might be related to the decrease of inflammatory
cytokines and the increase of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase,
glutathione S transferase, glutathione reductase), which would result in the reduction of iNOS,
COX-2 and MDA and subsequently inflammatory responses.