2.2.3. NO Release

**Figure 3.** Nitric oxide (NO) production from BV-2 cells (\*\*\* *p* < 0.001; \*\*\*\* *p* < 0.0001, *n* = 3). (**A**) Inflammation induced by various concentration of LPS (compared with control group), (**B**) cells treated with EGCG followed by LPS induction (compared with LPS (+) and EGCG (−)), (**C**) cells treated with EGCG, PC-EGCG-liposomes, and EGCG-VE-liposomes then LPS (compared with LPS (+)).

> NO release from BV-2 cells treated with 25 μM EGCG was not statistically significant compared to the control group, as shown in Figure 3B. However, the cell inflammation induced with LPS for 24 h showed a significant increase compared to the control group. Those cells treated with 25–200 μM EGCG for 1 h and then activated with LPS showed a statistically significant decrease compared to the group of cells activated with LPS only. NO release did not decrease when EGCG increased from 50–200 μM since the cell viability decreased when EGCG had risen from 50–200 μM, according to Figure 1A.

> The NO production of the cells treated with 25 μM EGCG followed by the inflammation induced with 50 ng/mL LPS was not statistically significant compared with the control group (Figure 3C). However, the NO released in the group of cells treated with PC-EGCG-liposomes or PC-EGCG-VE-liposomes followed by LPS activation with 50 ng/mL showed a significant decrease compared to the group of cells treated only with LPS. The NO release from cells pretreated with PC-EGCG-liposomes or PC-EGCG-VE-liposomes was higher than the NO release from the group of cells pretreated by EGCG, which should be explained by the slow release of EGCG from the liposomes.
