Fig 2: The levels of IL-1β, IL-6, and TNF-α in the cortical supernatant at specific time points. a IL-1β; b IL-6; c TNF-α. Data is represented by histograms. Values are expressed as mean ± SEM (n = 6 in each group. *P < 0.05 vs. sham group)

Fig 3: PQQ treatment alleviated sepsis-induced inflammation and oxidative stress. (a) Levels of IL-6, IL-1β and TNF-α in the serum of SD rats were detected using ELISA methods. (b) Expressions of IL-6, IL-1β and TNF-α in liver tissues of SD rats were detected by RT-qPCR assay. (c) The production of MDA and GSH in liver tissues of SD rats was detected with the commercial kits

Fig 4: The possible action mechanisms of zerumbone on the amelioration of DN in STZ-diabetic rats. Hyperglycemia induced p38 activation to augment the expression of ICAM-1and MCP-1, thereby enhanced the infiltration of monocytes and/or macrophages. The activated macrophages promoted the expression of inflammatory cytokines including TNFα, IL-1 and IL-6. All of the above abnormalities were reversed by zerumbone treatment. Zerumbone also decreased the expression of fibronectin, by reducing the TGF-β1 expression in the diabetic kidney.

Fig 5: Effects of pre-treatment with linalool (50 and 100 mg/kg) for 14 days on the inflammatory mediators (a) TNF-α, (b) NF-κB, (c) IL-1β, and (d) IL-6 in cisplatin-induced acute kidney injury. All values are expressed as mean ± SD. # indicates statistically significant from normal control group, * indicates statistically significant from cisplatin-only group, and @ indicates statistically significant from cisplatin + linalool 50 mg/kg group (p < 0.05) using one-way ANOVA followed by Tukey’s post-hoc test.