Catechin Weakens Diabetic Retinopathy by Inhibiting the Expression of NF-κB Signaling Pathway-Mediated Inflammatory Factors

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Abstract

Abstract.

Objective. The aim of the present study was to explore the role of catechin on the expression of heat shock protein 27 (HSP27), nuclear factor-kappa beta (NF-κB) and inflammatory factors IL-1β, IL-6 and TNF-α in streptozotocin (STZ)-induced diabetic retinopathy (DR) rats. Methods. A total of 150 rats were selected and randomly assigned to five groups: control group, STZ group, and three groups with different concentrations of catechin (low, middle and high concentrations). After STZ induction, DR rats were treated with different concentrations of catechin (50 mg/kg/day, low catechin group; 100 mg/kg/day, middle catechin group; 200 mg/kg/day, high catechin group) by intravitreal injection for eight weeks. Hematoxylin and eosin (H&E) staining was used to observe the pathological changes in retinal tissues. The mRNA and protein levels of HSP27 in the retina were determined by RT-PCR and western blotting. Furthermore, the expression of NF-κB p65 and p-NF-κB p65 were determined by western blotting, while the expression of IL-1β, IL-6, and TNF-α were determined by ELISA. Results. HSP27 levels increased in STZ-induced DR rats, and became further upregulated after catechin treatment. Furthermore, IL-1β, IL-6, and TNF-α levels were upregulated in the retinas of STZ-induced DR rats, but these changes were partially inhibited after treatment with catechin. Moreover, the application of catechin inhibited the activation of NF-κB, which was upregulated in STZ-induced DR. A negative correlation was observed between the concentrations of catechin and the expression of inflammatory factors. Conclusion. Catechin can weaken DR induced by STZ by increasing HSP27 levels and decreasing the production of associated inflammatory factors. This could help to treat DR in clinic.

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