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Fig. 1 | BMC Infectious Diseases

Fig. 1

From: Alpha7 nicotinic acetylcholine receptor is required for blood-brain barrier injury-related CNS disorders caused by Cryptococcus neoformans and HIV-1 associated comorbidity factors

Fig. 1

Effects of blockages of α7 nAChR and NF-κB on gp41-I90- and METH-induced monocyte transmigration across BBB. HBMECs were pre-incubated with or without gp41-I90 (10 μg/ml) and METH (50 nM) for 48 h, and then treated with different doses of inhibitors CAPE (0, 1 μM, 5 μM, 25 μM) for 2 h or MLA (0, 0.1 μM, 1 μM, 10 μM) for 1 h before the Monocytes transmigration assays. Freshly isolated monocyte-like vitamin D3-differentiated HL60 cells (1x106 cells) were added to the upper chamber and allowed to migrate over for 4 h. (a-b) CAPE (NF-κB inhibitor) could dose-dependently block gp41- and METH-induced monocyte transmigration across HBMEC. (c-d) MLA (α7 antagonist) was able to inhibit gp41- and METH-induced monocyte transmigration across HBMEC in a dose-dependent manner. Values represent the means of relative transmigrating monocytes of triplicate samples. In (a-d), the experimental setting without inhibitor treatment was taken as a control (the first column). Bar graphs showed the means ± SD of the triplicate samples. *P < 0.05, **P < 0.01

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