叶黄素通过调控自噬对高氧诱导的新生小鼠视网膜病变的治疗作用OA

Aim To investigate the therapeutic effect of lutein on hyperoxia-induced retinopathy in neonatal mice and elucidate its underlying mechanism.Meth-ods A 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 lu-tein 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;expres-sions of SIRT1 and PGC-1α in retinal tissues were de-tected by immunohistochemistry;expressions of LC3 and p62 were measured by immunofluorescence;and pathway-related protein levels were assessed by West-ern blot.Results Compared with the control group,the model group showed significant abnormalities in retinal vascular network morphology,including pro-nounced 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 de-creased(P<0.05).In contrast,all lutein treatment groups exhibited markedly restored retinal vascular network morphology and significantly reduced avascu-lar area compared with the model group.Moreover,the protein expression of p62 significantly decreased,while the expressions of AMPK,SIRT1,PGC-1α,LC3-Ⅱ,and the LC3-Ⅱ/LC3-Ⅰ ratio significantly in-creased(P<0.05).Conclusion Lutein demon-strates a significant therapeutic effect on hyperoxia-induced retinopathy in neonatal mice,likely mediated through promoting autophagy via regulation of the AMPK/SIRT1/PGC-1α signaling pathway.