Minocycline Regulates MCPIP1/NLRP3 Pathway and Inhibits Apoptosis in Diabetic Retinopathy

OBJECTIVE To investigate the effect of minocycline on MCPIP1/NLRP3 pathway in inhibiting apoptosis of diabetic retinopathy cells and its mechanism. METHODS Diabetic retinopathy(DR) mice models were prepared by intraperitoneal injection of streptozotocin, and then divided into model group and minocycline group, and set blank control group with no treatment. The retinal potential of mice was detected by electroretinogram(ERG). The expression levels of MCPIP1, NLRP3 and ASC in the retina of mice were detected by Western blotting. The number of apoptotic retinal cells was counted by TUNEL. Then the expression of NLRP3, ASC, IL-1β, IL-18 and caspase-1 treatment with minocycline and knockdown of MCPIP1 was detected by RT-PCR using high-sugar cultured human retinal pigment epithelium(RPE). RESULTS Compared with model group, following minocycline treatment, the amplitude of retinal potential in DR mice increased; the expression of MCPIP1 in the retina of DR mice was up-regulated, while the expression of NLRP3 and ASC was inhibited; the number of apoptotic retinal cells in DR mice decreased. Minocycline could promote the expression of MCPIP1 in RPE cultured with high glucose. Down-regulation of MCPIP1 reversed the inhibitory effects of minocycline on NLRP3, ASC, IL-1beta, caspase-1, IL-18. CONCLUSION Minocycline can inhibit NLRP3 by up-regulating MCPIP1, thus inhibiting or delaying diabetic retinopathy.