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Purpose  The aim of this study was to investigate the underlying mechanisms of diabetic retinopathy (DR) development.    Methods  Real-Time qPCR was used to detect  Casein kinase 2 interacting protein - 1  ( CKIP - 1 ) and  Nuclear factor E2 - related factor 2  ( Nrf2 ) mRNA levels. Western Blot was employed to detect protein levels. Malondialdehyde (MDA) assay kit, superoxide dismutase (SOD) kit and glutathione peroxidase (GSH-Px) kit were used to evaluate oxidative stress in high-glucose treated human retinal endothelial cells (HRECs). Calcein-AM/propidium iodide (PI) double stain kit was employed to detect cell apoptosis. Enzyme-linked ImmunoSorbent Assay (ELISA) was used to detect inflammation associated cytokines secretion. Co-immunoprecipitation (CO-IP) was performed to investigate the interactions between  CKIP - 1  and  Nrf2 . Luciferase reporter gene system was used to detect the transcriptional activity of  Nrf2 .    Results   CKIP - 1  was significantly downregulated in either DR tissues or high-glucose treated HRECs comparing to the Control groups. Besides, high-glucose (25 mM) inhibited HRECs viability and induced oxidative stress, inflammation associated cytokines (TNF-α, IL-6 and IL-1β) secretion and cell apoptosis, which were all reversed by synergistically overexpressing  CKIP - 1  and aggravated by knocking down  CKIP - 1 . Of note, we found that overexpressed  CKIP - 1  activated  Nrf2 / ARE  signaling pathway and increased its downstream targets including  HO - 1 ,  NQO - 1 ,  γGCS  and  SOD  in high-glucose treated HRECs. Further results also showed that  CKIP - 1  regulated cell viability, oxidative stress, inflammation and apoptosis in high-glucose treated HRECs by activating  Nrf2 / ARE  signaling pathway.    Conclusion  We concluded that overexpressed  CKIP - 1  alleviated DR progression by activating  Nrf2 / ARE  signaling pathway.

cell and bioscience

Upregulation of CKIP-1 inhibits high-glucose induced inflammation and oxidative stress in HRECs and attenuates diabetic retinopathy by modulating Nrf2/ARE signaling pathway: an in vitro study