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.