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. 2019 Oct 22;10:1245. doi: 10.3389/fphar.2019.01245

Figure 6.

Figure 6

The anti-inflammatory effect of CBL was abolished by a specific CREB inhibitor 666-15 compound in the primary mouse microglial cells, and 666-15 also attenuated the anti-ischemic effect of CBL. (A) 666-15 reduced protein expression of phosphorylated CREB (p-CREB) in primary mouse microlgia. Cells pre-incubated with 666-15 compound (1 μM) for 12 h were treated with 5 μg/mL CBL for another 3 h. (B) 666-15 compound attenuated the CBL enhancement of the protein expression of PGC-1α and p-CREB in primary microglia. Cells pre-incubated with 666-15 compound (1 μM) for 12 h were treated with 5 μg/mL CBL for another 3 h, and then added 100 ng/ml LPS for 2 h. (C) 666-15 compound reversed the CBL inhibition of pro-inflammatory factors gene expression and the promotion of anti-inflammatory factors gene expression. Results are shown as means ± SEM (n = 3). **P < 0.01, ***P < 0.001 versus the control group (CN); ##P < 0.01, ### P < 0.001 versus the CBL group or LPS group; $$P < 0.01, $$$P < 0.001 versus the LPS+CBL group. (D) The CREB inhibitor 666-15 compound reversed the anti-ischemic effect of CBL in rats subjected to tMCAO. Rats were first intraperitoneally injected with 10 mg/kg 666-15 compound for 30 min, followed by intravenous injection with 60 mg/kg CBL at 3 h and 24 h after ischemia, and brains were removed to test histological analysis at 72 h after ischemic stroke. N = 6, results are expressed as means ± SEM. ***P < 0.001 versus the Sham group; ###P < 0.001 versus the Stroke group; $$$P < 0.001 versus the Stroke+CBL group.