Fig. 2

α-DIPA inhibits LPS-induced microglia inflammation. (A) α-DIPA inhibits lipopolysaccharide (LPS)-induced microglial NO release in a concentration-dependent manner. BV-2 cells treated with 1.0 µg/mL LPS, and various concentrations (10, 20, 40, and 80 µM) of α-DIPA. BV-2 cells treated without LPS was used as negative control to detect baseline of NO release, while BV-2 cells treated with 100 µM L-NMMA, a total inhibitor of NO synthetase, was used as positive control. Five biological replicates for each group. (B-J) Treatment of 40 µM α-DIPA for 1 h significantly inhibited LPS-induced BV-2 cell proliferation (B), activation (C and D), as well as M1 type (E and F) and M2 type (G-J) polarization. CD68 marker was used for staining activated BV-2 cells (C and D). CCR7 marker was used for staining BV-2 cells with M1 type polarization (E and F). While double staining of CD206 and CD163 markers were used for detecting BV-2 cells with M2 type polarization (G-J). BV-2 cells were treated with 1.0 µg/mL LPS for 24 h in (B-J). MFI in (B), (D), (F), (H), and (J) denotes mean fluorescence intensity. Three biological replicates for each group in (B-J). Samples were compared using one-way ANOVA statistical analysis and Tukey’s multiple comparisons post-hoc test, *: p < 0.05, **: p < 0.01, ***: p < 0.001