Fig. 3

Hemin-induced inflammatory responses in the brain are compromised in TLR2 KO mice. a-b WT and TLR2 KO mice (n = 5 in each group) were administered 250 nmol of hemin in the striatum. After 24 h, the ICH-injured brains were dissociated into single-cell suspensions and the percentages of leukocytes (CD45^high), macrophages (CD45^high/CD11b⁺/Ly6G⁻), neutrophils (CD45^high/CD11b⁺/Ly6G⁺), and microglia (CD45^med/CD11b⁺) in the analyzed single cell population were determined using flow cytometry (*** p < 0.001 vs. hemin-injected WT mice). c-g Total RNA was isolated from the WT and TLR2 KO brain tissues (AP, 0.0 to −2.0 mm) 6 h after either saline- or hemin-administration, and used for quantitative real-time RT-PCR to measure CXCL1 (c), CXCL2 (d), IL-1β (e), IL-6 (f), and TNFα g mRNA levels. The mRNA levels of the hemin-injected mice were normalized to the levels of the saline-injected mice, and presented as fold induction (* p < 0.05, ** p < 0.01 vs. WT mice, n = 3). For all graphs, the data are presented as mean ± SEM