Objective To investigate the protective effect of TSLE on high fat induced retinal injury in rats and its mechanism. Methods A total of 24 male SD rats were randomly divided into normal group (N group), high fate (HF) group and HF + Toona Sinensis Leaves Extract (TSLE) group, 8 for each group. Rats in HF group and TSLE group were fed with high fat diet (10 ml/kg), and rats in normal group was given the same dose of normal saline. After 8 weeks, fasting blood lipids were measured in two groups. Rats in HF+TSLE group were fed with TSLE water solution (1 g/kg), rats in N group and HF group were given the same amount of normal saline. After TSLE intervention for 4 weeks, all rats were examined by flash electroretinogram (FERG). Blood levels of lipid and liver function were recorded. Morphological changes of retinal tissue were evaluated by HE staining. Immunohistochemistry and Western blot were performed for expression of IL-6, TNF-α, NF-κB p65, and caspase-3 protein in retina tissue. Results Serum levels of lipid levels including TC, TG, LDL-C and HDL-C were significantly different among groups; those in HF group were increased significantly when compared with those in N group (P < 0.05); those levels between N group and HF+TSLE group were not significantly different (P > 0.05) but significantly different between HF group and HF+TSLE group (P < 0.05). α wave latency among groups were statistically different (P < 0.05). No obvious differences in β wave incubation period, β wave, and α wave were observed among groups (P > 0.05). There was difference in α wave incubation period between HF group and N group or HF+TSLE group. Retinal thickness in HF group was significantly increased compared with N group (P < 0.05), which was diminished with treatment of TSLE (P < 0.05). The results of immunohistochemistry and Western blotting showed that the levels of IL-6, Caspase-3, TNF-α, and NF-κBp65 in HF group were significantly enhanced (P < 0.05), which were decreased by treatment with TSLE (P < 0.05). Conclusion TSLE protects high fat induced retinal damage through inhibiting the expression of IL-6, TNF-α, NF-κB p65 and Caspase-3.