METHODS: A total of 100 patients with T2DM treated in our hospital from July 2016 to December 2017 were assigned into T2DM patients with DR(DR group, n=32)and T2DM patients without DR(T2DM group, n=68). Thirty healthy volunteers were selected as control group. Real-time PCR was used to examine the expression of miR-146a. Enzyme linked immunosorbent assay was used to detect the levels of NF-κB and VEGF. The correlation between miR-146a and NF-κB and VEGF was analyzed.

RESULTS: Compared with the control group, HbA1c in T2DM group and DR group increased(t=6.822, 5.709; P<0.001), FBG increased(t=8.889, 7.923; P<0.001), 2hPBG increased(t=6.646, 5.514; P<0.001). Compared with T2DM group, the duration of diabetes in DR group was longer(t=2.431, P=0.017). Compared with the control group, serum miR-146a in T2DM and group DR significantly decreased(t=3.967, 7.169; P<0.001), and the DR group was lower than that in the T2DM group(t=4.444, P<0.001). Compared with the control group, the serum NF-κB in the T2DM and DR group increased significantly(t=6.063, 14.851; P<0.001), VEGF increased significantly(t=7.613, 12.943; P<0.001), NF-κB and VEGF in DR group were larger than those in T2DM group(t=11.406, 7.560; P<0.001). Pearson analysis showed that miR-146a was negatively correlated with NF-κB and VEGF(r=-0.503, -0.574; P<0.05).

CONCLUSION: The serum miR-146a in DR patients significantly decreased, the NF-κB and VEGF significantly increased. MiR-146a may be involved in the pathogenesis of DR by mediating inflammatory reaction and vascular proliferation.