The therapeutic effect of lutein on hyperoxia-induced retinopathy in neonatal mice through regulating autophagy

AimTo investigate the therapeutic effect of lutein on hyperoxia-induced retinopathy in neonatal mice and elucidate its underlying mechanism.MethodsA murine model of retinopathy was established by hyperoxia induction in newborn C57 mice. After successful modeling, the mice were randomly divided into model group, model + low-/medium-/high-dose lutein groups(1, 10, and 100 mg·kg-1), and normal control group. Retinal histopathology was examined by HE staining; retinal vascular network morphology and angiogenesis were observed via ADP staining; expressions of SIRT1 and PGC-1α in retinal tissues were detected by immunohistochemistry; expressions of LC3 and p62 were measured by immunofluorescence; and pathway-related protein levels were assessed by Western blot.ResultsCompared with the control group, the model group showed significant abnormalities in retinal vascular network morphology, including pronounced vascular dilation and structural distortion. The protein expression of p62 significantly increased, while expressions of AMPK, SIRT1, PGC-1α, LC3-Ⅱ, and the LC3- Ⅱ/LC3- Ⅰ ratio significantly decreased (P P ConclusionLutein demonstrates a significant therapeutic effect on hyperoxiainduced retinopathy in neonatal mice, likely mediated through promoting autophagy via regulation of the AMPK/SIRT1/PGC-1α signaling pathway.