Fig. 5.

Suppression of TNTL on MIP1γ secretion from macrophages mediated its improvement on endothelial condition in retina. a. showed that antibody array on serums from hyperglycemic mice with or without TNTL treatment (0.9 g/kg); b. showed that antibody arrays on SN from BMDMs with or without TNTL treatment (20 mg/mL). The red squares highlighted cytokines suppressed by TNTL while the blue squares indicated cytokines provoked by TNTL; c. showed that IL4, GM-CSF, and MIP1γ were significantly regulated in both serum and SN; d. showed that expression of MIP1γ but not GM-CSF could be significantly suppressed in pro-inflammatory BMDMs by TNTL; e. showed that supplementation of MIP1γ in SN from TNTL-treated BMDMs recovered its ability in attracting RECs migration; f. showed that supplementation of MIP1γ in SN from TNTL-treated BMDMs recovered its ability in destroying RECs monolayer integrity; g. showed that supplementation of MIP1γ in SN from TNTL-treated BMDMs recovered its ability in inducing FITC leakage through RECs monolayer. *p < 0.05, **p < 0.01, ***p < 0.001 when compared with model group