Found programs: Natural Science Research Project of Anhui Educational Committee (No . 2022AH050651) ; Sci- entific Research Project of Anhui Medical University ( No . 2022xkj107) ; Natural Science Key Project of Bengbu Medical University (No . 2022byzd196) .
Authors：Zhang Lei 1 , 2 , Zhang Sumei3 , Yang Zhen3 , Hu Weikang3 , Bai Hongmei3 , Zhou Wenjing3 , Wang Zihan3 , Li Mingcong4 , Zhang Shengquan3 , Liao Rongfeng1
Keywords：high throughput sequencing; laminarin; diabetes retinopathy; C57 BL/6
DOI：10.19405/j.cnki.issn1000-1492.2025.03.002
〔Abstract〕 Abstract Objective To investigate the effect of laminarin(LAM) on nonproliferative diabetes retinopathy by high throughput sequencing( RNA-seq) . Methods The diabetes model was established by intraperitoneal injection of streptozotocin (STZ) , and the effect of LAM on diabetic mice was observed . C57BL/6 mice were randomly divided into three groups : control group , model group , and LAM group , with 8 mice in each group . After 8 weeks of model- ing , the LAM group received a 4-week intraperitoneal injection of LAM treatment. Changes in blood glucose and body weight of the three groups of mice were recorded , HE staining was performed to examine retinal lesions , and RNA-seq was used to identify differentially expressed genes (DEGs) in DR under the action of STZ and LAM . Re- sults STZ successfully established the model of diabetic retinopathy (DR) , and LAM reduced the blood sugar in diabetic mice to a certain extent and improved the pathological morphology of retinal structural looseness in diabetic mice . After RNA-seq analysis of DEGs , it was found that there were a total of 214 DEGs in the retina of the Model group mice compared to the Control group . Enrichment analysis revealed that DR could exacerbate the lesions through the PI3K Akt signaling pathway . There were a total of 42 DEGs in the retina of the Model group and LAM group mice , and enrichment showed that LAM improved the lesions through the neutrophil extracellular trap path- way . Early growth response factor 1 (EGR1) , FBJ osteosarcoma oncogene (Fos) , nuclear receptor subfamily 4A member 1 (NR4A1) , and salt-induced kinase 1 (SIK1) were regulated by STZ , and LAM significantly regulated their expression , which might be closely related to LAM ′s treatment of diabetic retinopathy . Conclusion DEGs can exacerbate the severity of diabetic retinopathy via the PI3K-Akt signaling pathway . LAM can mitigate diabetic reti- nopathy via the neutrophil extracellular trap pathway . Egr1 , Fos , Nr4a1 , and Sik1 are key genes involved in lami- narin ′s treatment of STZ-induced diabetic retinopathy .