Fig. 6

LAM treatment significantly decreased microglial activation in the ischemic mice and inhibited TNF-α and iNOS expression in the ischemic brain tissue and OGD/R-induced BV2 cells. a, b Microglial activation was assessed by Iba-1 and CD68 staining, and Iba-1- and CD68-positive cells were significantly increased in the ischemia and ischemia + saline groups. LAM treatment significantly attenuated microglial activation (scale bar, 50 μm; n = 3/group; ^*P < 0.05 vs. sham group; ^#P < 0.05 vs. ischemia group/ischemia + saline group). c, d TNF-α and iNOS expression was significantly enhanced in the ischemia and ischemia + saline groups compared with that of the sham group, and LAM treatment significantly inhibited TNF-α and iNOS expression in the ischemia group compared with that of the ischemia and ischemia + saline groups (n = 3/group; ^*P < 0.05 vs. sham group; ^#P < 0.05 vs. ischemia group/ischemia + saline group). However, no significant difference was observed between the ischemia group and ischemia + saline group. e, f TNF-α and iNOS expression was significantly increased in BV2 cells subjected to OGD/R for 3 h compared with that of cells without OGD/R exposure. LAM pretreatment of BV2 cells with OGD/R exposure significantly decreased the expression of the aforementioned proteins (n = 3/group; ^*P < 0.05 vs. control group; ^#P < 0.05 vs. OGD/R group).