*2.3. RI Attenuated the LPS-Induced NO and ROS Production in RAW 264.7 Cells*

In LPS-treated cells, there was a marked increase (*p* < 0.05) in NO and ROS production as compared to the control. Conversely, co-treatment with the RI significantly reduced (*p* < 0.05) the NO and ROS production in a dose-dependent manner (Figure 2a,b). Together, RI suppressed the LPS-induced inflammatory response by preventing NO and intracellular ROS production in RAW 264.7 cells.

**Figure 2.** Protective role of RI on NO, intracellular ROS and MDA production in RAW 264.7 cells and gastric tissue. (**a**) NO; and (**b**) ROS production was measured by Griess and ROS-Glo H2O2 assays in RAW 264.7 cells (upper panel). Cells were pretreated with various concentration of RI (100, 200, and 400 μg/mL) for 1 h, followed by co-treatment with RI and LPS (0.5 μg/mL) for another 24 h. (**c**) NO; and (**d**) MDA production in gastric tissue were measured by Griess and TBARS assays (lower panel). Mice were pretreated for 1 h with RI (400 mg/kg) and Ranitidine (40 mg/kg). After 1 h, HCl/EtOH (10 μL/g) was given orally. # *p* < 0.05 when compared with the control and \* *p* < 0.05 when compared with LPS and HCl/EtOH. Data are expressed as mean ± SEM.
