Fig 1: Effects of MCP-1 neutralization on MIP-2 and 67LR expressions in the FPC following SE. As compared to control IgG, MCP-1 neutralization ameliorates MIP-2 induction and increases 67LR expression in astrocytes. (A) Representative photos of MIP-2 and 67LR expressions in the FPC following SE. (B) Quantification of the MIP-2 intensity in astrocytes (n = 40 cells in 7 rats, respectively). * p < 0.05 vs. control IgG (n = 7 rats, respectively). (C) Quantification of the MIP-2 mRNA in the hippocampus. *,# p < 0.05 vs. control animal and vehicle, respectively (n = 4 rats, respectively). (D) Quantification of 67LR intensity in astrocytes. * p < 0.05 vs. control IgG (n = 40 cells in 7 rats, respectively).
Fig 2: A schematic diagram of the underlying mechanisms of the effect of EGCG on SE-induced leukocyte infiltration. SE led to NF-κB-mediated MCP-1 induction in microglia, which was attenuated by EGCG. Released MCP-1 from microglia recruited blood-derived monocytes and activated MIP-2 upregulation in astrocytes via the CCR2-67LR-ERK1/2 signaling pathway. EGCG and U0126 also attenuated MIP-2 induction in astrocytes by facilitating 67LR-mediated ERK1/2 inactivation, which ameliorated neutrophil/monocyte infiltration.
Fig 3: Effects of 67LR neutralization and co-treatment of EGCG or U0126 on leukocyte infiltration, MIP-2 expression and p-ERK1/2 level in the FPC under physiological condition. Although 67LR neutralization does not alter 67LR expression, it induces MIP-2 induction, leukocyte infiltration and p-ERK1/2 upregulation in the FPC without MCP-1 induction, which are ameliorates by co-treatment of EGCG or U0126. (A) Representative photos of 67LR, MCP-1, MIP-2 and p-ERK1/2 expressions in the FPC induced by 67LR neutralization. (B) Quantification of the number of infiltrating leukocytes. * p < 0.05 vs. vehicle co-treatment (n = 7 rats, respectively). (C) Quantification of MIP-2 and p-ERK1/2 levels in astrocytes. *,#p < 0.05 vs. co-treatment (n = 40 cells in 7 rats, respectively). (D) Quantification of the MIP-2 mRNA in the hippocampus. *,#,$ p < 0.05 vs. control, vehicle and EGCG, respectively (n = 4 rats, respectively).
Fig 4: SE-induced MIP-2 induction and cellular localization of MIP-2. SE induces MIP-2 expression in reactive astrocytes and a few neurons. EGCG attenuates astroglial MIP-2 upregulation induced by SE. (A) Representative photos of astrocytes (GFAP), MIP-2 expression and MIP-2 intensity in the FPC. (B) Representative photos of CCR2 expression in a few neurons. (C) Quantification of the MIP-2 intensity in astrocytes. * p < 0.05 vs. vehicle (n = 40 cells in 7 rats, respectively). (D) Quantification of the MIP-2 mRNA in the hippocampus. *,# p < 0.05 vs. control animal and vehicle, respectively (n = 4 rats, respectively).
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