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. 2020 Nov 7;11(3):708–726. doi: 10.1016/j.apsb.2020.11.002

Figure 6.

Figure 6

SIRT6 activator MDL-811 ameliorates brain ischemic injury and neuroinflammation in tMCAO mice. MDL-811 (1 or 10 mg/kg) reduced brain infarct size (A and B) and ameliorated neurological deficits evaluated by Longa test and corner test (C) after mice were subjected to tMCAO for 72 h (n = 8). Data are representative of two independent experiments. (D) Representative double-staining immunofluorescence of IBA1 (green) and CD16 (red) in the peri-infarct areas of the brain sections. (E) Quantification of IBA1+ CD16+ cells in the peri-infarct areas of the ischemic brains (n = 3). MDL-811 significantly reduced the mRNA levels of pro-inflammatory factors, including CD16 (F) Tnf-α and Il-1β (G), and enhanced anti-inflammatory factors mRNA expressions, including arginase1 and CD206 (H) in the cortex of peri-infarct region at 72 h after mice were subjected to tMCAO (n = 8). Results were normalized to 18S rRNA. Data are representative of three independent experiments. Western blot analysis (I and J) on the expression of SIRT6, H3K9Ac and H3K56Ac in the peri-infarct cerebral cortex region of mice at 72 h post tMCAO treated with or without MDL-811 (n = 4). H3 is the internal control and β-actin is the loading control. Data are representative of three independent experiments. Results in this figure are expressed as mean ± SEM; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 versus the sham group; #P < 0.05, ##P < 0.01, ###P < 0.001 versus the vehicle group.