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AIM: To study the protective effect of fenofibrate on diabetic retinal neurodegeneration and observe its effect on miR-26a-5p and its target gene PTEN in the retinal of diabetic mice.METHODS: Diabetic mice models were established and they were gavaged by fenofibrate. H& E staining and transmission electron microscopy were used to observe the impairments of retinal neurons. Real-time PCR was used to examine the expression of miR-26a-5p, and Western blotting was employed to measure the expression of phosphatase and tensin homologue(PTEN)in the retina of diabetic mice. The expression level of nuclear factor-κB(NF-κB), interleukin-1β(IL-1β)and the morphology of neural tissues were observed.RESULTS: When compared with the diabetic mice, fenofibrate significantly attenuated the damage to retinal ganglion cells and the atrophy of retinal nerve fiber layer. While the level of miR-26a-5p was increased and the levels of PTEN and inflammatory mediators were significantly decreased in the retina of fenofibrate treated diabetic mice, with significant statistical significance(P<0.05).CONCLUSIONS: Fenofibrate protects against diabetic retinal neurodegeneration by upregulating miR-26a-5p and inhibiting PTEN, attenuating the inflammatory response and alleviating retinal cell injury.
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@#Diabetic retinopathy(DR)has always been considered as microangiopathy. However, a large number of studies have confirmed that DR can not only cause retinal angiopathy, but also cause retinal neurodegeneration. Recently, more and more evidence also shows that retinal neurodegeneration occurred before retinal angiopathy in the early stage of DR, and retinal neurodegeneration may be involved in the occurrence and development of microvascular abnormalities. At present, the mechanism of diabetic retinal neurodegeneration is not very clear. This paper reviews the research progress on the mechanism of diabetic retinal neurodegeneration in recent years.