To investigate the effect of Maresin1 (MaR1) on retinal neuroinflammation in diabetic (DM) rats and its mechanism. Mtehods: Forty SD rats were randomly divided into 4 groups: the control (Con) group, diabetes (DM) group, Maresin1 (MaR1) group, and Maresin1 + colivelin (Colivelin) group. Intraperitoneal injections of streptozocin (STZ) were given to establish the rat DM model. After model creation, the MaR1 group was given intraperitoneal injections of MaR1 (4 ng/g) 2 times per week, and the Con and DM groups were given equal volume injections of PBS. The Colivelin group rats, in addition to receiving the same injections as MaR1 group rats, were anesthetized then given an intravitreal injection of 5 μL of colivelin (10 － 4 μmol L-1). Samples were collected after 12 weeks. HE staining was used to visualize histopathological changes in retinal tissue. Immunohistochemistry was used to evaluate the expression of glial fibrillary acidic protein (GFAP) in the retina. The levels of retinal IL-6, IL-1β, and TNF-α were assessed by ELISA. The expression level of retinal IL-6, IL-1β, TNF-α, and JAK2/STAT3 signaling proteins were found by Western blot. Results: Compared to the Con group, the DM group showed a significantly decreased retinal ganglion cell (RGC) number, increased GFAP expression, and increased IL-6, IL-1β, TNF-α, p-JAK2, and p-STAT3 expression (P<0.01). Compared to the DM group, the MaR1 group showed an increased number of RGC, decreased GFAP expression, and decreased IL-6, IL-1β, TNF-α, p-JAK2, and p-STAT3 expression (P<0.01). Compared to the MaR1 group, the Colivelin group showed a decreased RGC number, increased GFP expression, and increased IL-6, IL-1β, TNF-α, p-JAK2, and p-STAT3 expression (P<0.01). The protective effect of MaR1 on the retina of DM rats was reversed when colivelin, a JAK2/STAT3 pathway activator, was administered. Conclusion: MaR1 has a certain inhibitory effect on retinal inflammation in diabetes rats, which may be related to the inhibition of JAK2/STAT3 pathway.