The antioxidant effects of G-Rh1 are summarized in [ Table 3 ]. It was shown that pretreatment with G-Rh1 at the concentrations of 100 µM and 300 µM for 1 h significantly suppressed ROS production in BV2 cells stimulated by LPS ( µg/mL) [ 50 ] or IFN- γ (100 U/mL) [ 37 ]. On myocardiocytes from Wistar rats, G-Rh1 (30 µM) decreased the free radical content of myocardiocytes by more than 50% after incubation with xanthine-xanthine oxidase for 5 days [ 51 ]. Using the 2′,7′,-dichlorofluorescin diacetate assay, the intracellular ROS scavenging activity of G-Rh1 was determined to be 45% at 10 µM compared to 90% in the case of the same dose of N-acetylcysteine as a positive control [ 52 ]. He et al. [ 53 ] compared the inhibitory effects of five ginsenosides (Rb1, Rb2, Rd, Rh1, Rh2) on superoxide generation induced by fMLP, PMA, and arachidonic acid in human neutrophils. They found that G-Rh1 slightly suppressed PMA- and arachidonic acid-induced superoxide generation, but strongly inhibited the fMLP-stimulated process at a higher extent than the four other ginsenosides. Moreover, it exhibited almost no effect on the lipid peroxidation level concentrations up to 200 µM, suggesting the mechanism of action is to suppress stimulus-induced superoxide generation of neutrophils rather than scavenge generated free radicals. They also performed experiments with the DPPH assay and confirmed that G-Rh1 did not possess a scavenging effect. To explain this, Chae et al. [ 52 ] supports that the DDPH assay is not an appropriate method to identify antioxidant effects of ginsenosides because they are not electron-rich compounds to donate their electron to DPPH. Their antioxidant ability should be examined through measuring the activity of free radicals, hydroxyl, ROS, etc.