Figure 2.
P7C3 inhibited LPS-induced transcriptional activation of pro-inflammatory factors in BV2 cells. (A) BV2 cells were pretreated with P7C3 (0.1, 1, or 10 μM) for 2 h and then exposed to LPS (100 ng/mL) for 6 h. After treatment, cell lysate was collected to measure the mRNA levels of iNOS, COX-2, IL-6 and TNFα using qRT-PCR assays. The values are presented as the means ± SEM from three independent experiments. Kruskal–Wallis test followed by the Iman-Conover method for multiple comparison between groups was performed, *P < 0.05, **P < 0.01 vs. the group treated with LPS. (B) BV2 cells were pretreated with P7C3 (10 μM) for 2 h and then exposed to LPS (100 ng/mL) for 6 h. After culture, cell lysate was collected and the mRNA levels of Arg1, IL-10, CD206 were measured using qRT-PCR assays. (C) BV2 cells were administrated with P7C3 (10 μM) for 2 h followed by IL-4 (20 ng/mL) treatment or IL-4 (20 ng/mL) plus LPS (100 ng/mL) treatment for 6 h. The mRNA levels of Arg1, IL-10, CD206 in cell lysate were detected. The data from three independent experiments were presented as the means ± SEM.; Kruskal–Wallis test followed by the Iman-Conover method for multiple comparison between groups was performed. ns, not significantly different.