Protective mechanism of lutein combined with EGCG against N-methyl-N nitrosourea-induced retinitis pigmentosa

In this study, N-methyl-N nitrosourea (MNU)-induced retinitis pigmentosa (RP) model mice were used to investigate the protective effect of lutein (LUT) combined with epigallocatechin-3-gallate (EGCG) treatment. Compared to the LUT group, after the LUT combined with EGCG (LUT-EGCG) treatment, the accumulation content of LUT was significantly increased by 50.24% in the liver. The histopathological results showed that LUT-EGCG treatment significantly improved the structural damage of the retina and recovered the thickness of the outer nuclear layer of the retina to 185.28 ± 0.29 μm, which was no significant difference compared to the control group. The LUT-EGCG treatment also increased the production of short-chain fatty acids such as acetic and propionic acids. Compared with LUT individual treatment, the LUT-EGCG treatment significantly increased the relative abundance of Lachnospiraceae and Helicobacteraceae by Metastats analysis. RT-qPCR results showed that LUT-EGCG treatment significantly increased the antiapoptotic gene Bcl-2 expression. In addition, the expression level of IL-6 in the LUT-EGCG group was down-regulated significantly, but there was no significance in NF-κβ, TNF-α, IL-1β, and IL-18 compared with LUT treatment. Coupled with correlation analysis, results showed that LUT combined EGCG might protect against RP by regulating antiapoptotic gene expression and improving intestinal flora. These results provided helpful information for RP intervention.