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The present report evaluates the protective effects of luteolin against diabetic retinopathy (DR).

Materials and methods

Diabetes was induced in rats by i.p. administration of 60 mg/kg of streptozotocin (STZ), followed by treatment with luteolin for 4 weeks. The effects of luteolin were determined based on the blood glucose and cytokine levels, and parameters of oxidative stress in retinal tissue of DR rats. The diameter of retinal vessels was estimated by fundus photography. A Western blot assay was used to determine the expression of apoptotic proteins and Nod-like receptor 3 (NLRP3) pathway proteins in the retina of DR rats. A molecular docking study was performed to evaluate the interaction between luteolin and NLRP3.


The level of blood glucose was reduced in the luteolin-treated group compared with the DR group. Reductions in cytokines and oxidative stress were observed in the retinal tissues of the luteolin-treated group relative to the DR group. Moreover, treatment with luteolin reduced the expression of NLRP1, NOX4, TXNIP, and NLRP3 proteins, and ameliorated the altered expression of apoptotic proteins in the retina of DR rats.


In conclusion, luteolin prevents retinal apoptosis in DR rats by regulating the NLRP/NOX4 signalling pathway.

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Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.

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