Abstract
Diabetic retinopathy (DR) is a kind of irreversible visual impairment common in adults. Several studies have confirmed the ability of fenofibrate (FNB) to mitigate DR pathology. miR-21 has also been shown to improve the hemodynamics of DR model rats. Presently, it is not clear whether FNB can play a therapeutic role in DR via regulating miR-21, and we will supplement this gap through this research. First, in this research, we constructed an in vitro model of DR by inducing ARPE-19 cells with high glucose (HG). After successful induction, the proliferation ability of ARPE-19 cells was inhibited, the apoptosis ability was enhanced, and the oxidative stress index (reactive oxygen species, ROS) level was increased. Subsequently, we discovered that the cell vitality was significantly improved, the apoptosis ability was inhibited, and oxidative stress injury was improved under FNB intervention in the in vitro model of DR. In mechanism, FNB can improve the viability of DR model in vitro and alleviate the oxidative stress injury induced by HG through down-regulating miR-21 or up-regulating IL-6R. Furthermore, miR-21 has a targeted regulatory relationship with IL6R, which can negatively regulate the level of IL6R. Based on the above, we conclude that FNB can improve the viability and alleviate oxidative stress injury of DR model in vitro via regulating the miR-21-IL6R axis.
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