Fig 2: Anti-inflammatory effect of UCF-101 in pneumonia. The levels of TNF-α, IL-1β, IL-6 and MCP-1 were measured with ELISA. Data are expressed as mean ± standard deviation (n=8). ***P<0.001 vs. control, ###P<0.001 vs. the LPS+DMSO group. TNF-α, tumor necrosis factor α; IL, interleukin; MCP-1, monocyte chemo-attractant protein-1; LPS, lipopolysaccharide; UCF-101, 5-[5-(2-nitrophenyl)furfuryl iodine]-1,3-diphenyl-2-thiobarbituric acid.

Fig 3: BMT of PTE-treated diabetic HSCs accelerates diabetic wound healing by ameliorating diabetes-induced oxidative stress and inflammation. Experimental rats were randomly separated into 4 groups as follows: rats with BMT of HSCs from CTL/VEH (BMT-CTL/VEH); rats with BMT of HSCs from STZ/VEH (BMT-STZ/VEH); rats with BMT of HSCs from STZ/RSV (BMT-STZ/RSV); and rats with BMT of HSCs from STZ/PTE (BMT-STZ/PTE). The rats were subjected to a model of cutaneous burn injury and the wound-healing process was evaluated, followed by biomedical analysis. (a) Superoxide anion release from wound tissues, n = 5. (b) IL1β in serum, n = 5. (c) IL6 in serum, n = 5. (d) MCP1 in serum, n = 5. (e) MCP1 quantitation by IHC from wound tissues on day 21, n = 5. (f) Representative pictures for (e). (g) Deposition of granulation cells from (h), n = 8. (h) H&E staining of wound tissues on day 21 after burn injury with occurrence of granulation cells in the wounds. (i) Representative pictures for evaluation of vascularity (assessed by CD31 IHC) for (j). (j) Numbers of CD31-positive vessels per high-power field on day 21 after burn injury, n = 8. (k) Photographs of representative wounds on day 21 after burn injury. (l) Graphical depiction of wound areas on different days after burn injury, n = 8. (m) Quantitation of burn area on day 21, n = 8. For bars in graphs marked with an asterisk, p < 0.05 vs CTL/VEH group. Data are expressed as mean ± SEM. BMT bone marrow transplantation, PTE pterostilbene, HSCs hematopoietic stem cells, CTL control, VEH vehicle, STZ streptozotocin, RSV resveratrol, IL1β interleukin-1β, IL6 interleukin-6, MCP1 monocyte chemoattractant protein-1, IHC immunohistochemistry

Fig 4: Activation of Nrf2 prevents diabetes-induced oxidative stress and expression of proinflammatory cytokines in rats. The burn injuries were introduced, and the experimental rats were divided into four groups: control rats (CTL/VEH), STZ diabetic rats (STZ/VEH), STZ rats treated by 15 mg/kg/d of DMF (STZ/DMF), or CTL rats received 15 mg/kg/d of ML385 (CTL/ML385). The wounds were excised and collected from the experimental rats for further analysis. (A) Superoxide anion release, n = 5. (B) mRNA levels for Nrf2 and its target genes by qPCR, n = 4. (C) Representative pictures for Western blots. (D) Protein quantitation for (C), n = 4. (E) Representative pictures for NQO1 expression by immunohistochemistry. (F) Representative pictures for HO1 expression by immunohistochemistry. (G) mRNA levels for proinflammatory cytokines, n = 4. (H) IL1β in serum, n = 5. (I) IL6 in serum, n = 5. (J) MCP1 in serum, n = 5. *P < 0.05, vs CTL group; ¶P < 0.05, vs STZ/VEH group. Data were expressed as mean ± SEM.

Fig 5: Nrf2 activator DMF prevents, while Nrf2 blocker ML385 mimics, hyperglycemia-induced expression of proinflammatory cytokines. Rat macrophage cells were treated by either 5 µM Nrf2 activator DMF or 5 µM Nrf2 inhibitor ML385, then incubated in either low glucose (5 mM) or high glucose (25 mM glucose) continuously for 5 days, and the cells were harvested on day 5 for further analysis. (A) mRNA levels by qPCR, n = 4. (B) IL1β secretion, n = 5. (C) IL6 secretion, n = 5. (D) MCP1 secretion, n = 5. *P < 0.05, vs LG/VEH group; # P < 0.05, vs HG/VEH group. Data were expressed as mean ± SEM.