Figure 1.

PTE has a stronger effect than RSV on accelerating diabetic wound healing by ameliorating diabetes-induced epigenetic modifications on the ERβ promoter in HSCs. Experimental rats with burn injuries were divided into 4 groups: control rats (CTL/VEH), STZ diabetic rats (STZ/VEH), STZ rats treated with 15 mg/kg/day of RSV (STZ/RSV) and STZ rats treated with 15 mg/kg body weight of PTE. (a) Photographs of representative wounds on day 15 post-burn. (b) Quantitation of burn area on day 15 post burn, n = 8. (c) Graphical depiction of wound areas on different days post-burn, n = 8. (d–g) HSCs were collected from treated rats for biomedical analysis. (d) mRNA levels determined by qPCR, n = 4. (e) Protein quantitation by WB for (f), n = 5. (f) Representative picture for western blots. (g) ChIP analysis on ERβ promoter, n = 4. (h–k) PBMCs were collected from treated rats for biomedical analysis. (h) mRNA levels by qPCR, n = 4. (i) Protein quantitation by WB for (j), n = 5. (j) Representative picture for western blots. (k) ChIP analysis on ERβ promoter, n = 4. For bars in graphs marked with an asterisk, p < 0.05 vs CTL/VEH group; for paragraph marks, p < 0.05 vs STZ/RSV group. Data are expressed as mean ± SEM. PTE pterostilbene, RSV resveratrol, ERβ estrogen receptor β, HSCs hematopoietic stem cells, CTL control, VEH vehicle, STZ streptozotocin, PBMCs peripheral blood mononuclear cells, NRF1 nuclear respiratory factor-1, SOD2 superoxide dismutase 2, H3K9me2 histone H3 lysine 9 dimethylation, H3K9me3 histone H3 lysine 9 trimethylation, H3K27me2 H3 lysine 27 dimethylation, H3K27me3 H3 lysine 27 trimethylation