Sirtuin

The eect of Melatonin, luzindole, and EX527 treatment on apoptotic index, infarct size, lactate dehydrogenase (LDH) release, and CK release in IR-injured hearts. Representative photomicrographs of in situ detection of apoptotic myocytes by TUNEL staining. Green fluorescence shows TUNEL-positive nuclei; blue fluorescence shows nuclei of total cardiomyocytes; original magnification 9x400. Sacle bar: 100 um.

Cellular senescence and SIRT1 phosphorylation was monitored in PAECs (P2) incubated in DMEM containing HDL (50 mg/L), LDL (50 mg/L), or resveratrol (100 μM) for 24 hours.

Effects of sirtinol on SIRT1 expression and HIF-1α. hMSCs were treated with sirtinol (100 uM) or equivalent concentration of DMSO (CTR) for 24 h and then exposed to 1% O2 for 6 h. All cells lysates were analyzed for SIRT1, HIF-1α, and tubulin by Western blot.

Immunoprecipitation-western blot for analyzing acetylated Snail in Snail-transfected 293T cells (upper) and FaDu-Snail cells (lower) treated with a vehicle control (Ctrl), a HDAC inhibitor TSA 5 nM for 8 hr, a SIRT1 inhibitor NAM(Nicotinamide) 10 mM for 8 hr, or in combination.

The SIRT1 inhibitor (tenovin-1) partially blocked the protective effect of γ-man in L02 cells. The effect of tenovin-1 on expression and acetylation level of PGC-1α (B) in L02 cells treated with or without γ-man.

Masson trichrome staining of tubulointerstitium areas from Sham, UUO, UUO+AGK2 mice (original magnification: × 400).

Effects of HNK or 3‐TYP on surgery/anesthesia‐induced an increased expression of pro‐inflammatory cytokines in hippocampus. (A, E) Representative blots at postoperative 1 and 3 d, respectively. (B, F) MCP‐1 relative expression. (C, G) TNF‐α relative expression. (D, H) IL‐1β relative expression. The data are presented as the mean ±standard error of the mean for each group (n = 6 per group). *P < 0.05 vs the control group; #P < 0.05 vs the surgery+vehicle group; $P < 0.05 vs the honokiol group

PAI-1 expression in HUVECs treated with drugs as indicated.(D) senescent HUVECs were treated with SRT1720, culturing for 24, 48 hours. PAI-1 mRNA and protein (E) levels were analyzed using real-time RT–PCR and Western blotting, respectively. The RNA and protein levels were normalized to the internal control β-actin. Data are presented as the mean±SEM of three independent experiments. *P < 0.05 vs. corresponding control. **P < 0.01 vs. corresponding control ***P < 0.001 vs. corresponding control.

After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of Quercetin for 3h,followed by 20-minute stimolation of 100ng/ml EGF.

Liver pathology and serum markers of liver injury in mice fed control (Ctrl), or ethanol (EtOH), or ethanol combined with fisetin (E/Fisetin) diet for 4 weeks. (A) Light microscopy with hematoxylin and eosin staining shows lipid accumulation (arrows) in the liver of mice after alcohol exposure, which was alleviated by fisetin administration. (B) Plasma alanine aminotransferase (ALT) and (C) aspartate aminotransferase (AST) activities. Infinity ALT and AST reagents were used formeasuring ALT and AST activities. Scale bar: 50 lm. Results are mean±SD (n = 3 to 6). Results for bars that do not share a letter differed significantly among groups (p < 0.05). Significant differences among groups are determined by analysis of variance followed by Tukey’s test.

After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of Quercetin for 3h,followed by 20-minute stimolation of 100ng/ml EGF.

The eect of Melatonin, luzindole, and EX527 treatment on apoptotic index, infarct size, lactate dehydrogenase (LDH) release, and CK release in IR-injured hearts. Representative photomicrographs of in situ detection of apoptotic myocytes by TUNEL staining. Green fluorescence shows TUNEL-positive nuclei; blue fluorescence shows nuclei of total cardiomyocytes; original magnification 9x400. Sacle bar: 100 um.

Cellular senescence and SIRT1 phosphorylation was monitored in PAECs (P2) incubated in DMEM containing HDL (50 mg/L), LDL (50 mg/L), or resveratrol (100 μM) for 24 hours.

Effects of sirtinol on SIRT1 expression and HIF-1α. hMSCs were treated with sirtinol (100 uM) or equivalent concentration of DMSO (CTR) for 24 h and then exposed to 1% O2 for 6 h. All cells lysates were analyzed for SIRT1, HIF-1α, and tubulin by Western blot.

Immunoprecipitation-western blot for analyzing acetylated Snail in Snail-transfected 293T cells (upper) and FaDu-Snail cells (lower) treated with a vehicle control (Ctrl), a HDAC inhibitor TSA 5 nM for 8 hr, a SIRT1 inhibitor NAM(Nicotinamide) 10 mM for 8 hr, or in combination.

The SIRT1 inhibitor (tenovin-1) partially blocked the protective effect of γ-man in L02 cells. The effect of tenovin-1 on expression and acetylation level of PGC-1α (B) in L02 cells treated with or without γ-man.

Masson trichrome staining of tubulointerstitium areas from Sham, UUO, UUO+AGK2 mice (original magnification: × 400).

Effects of HNK or 3‐TYP on surgery/anesthesia‐induced an increased expression of pro‐inflammatory cytokines in hippocampus. (A, E) Representative blots at postoperative 1 and 3 d, respectively. (B, F) MCP‐1 relative expression. (C, G) TNF‐α relative expression. (D, H) IL‐1β relative expression. The data are presented as the mean ±standard error of the mean for each group (n = 6 per group). *P < 0.05 vs the control group; #P < 0.05 vs the surgery+vehicle group; $P < 0.05 vs the honokiol group

PAI-1 expression in HUVECs treated with drugs as indicated.(D) senescent HUVECs were treated with SRT1720, culturing for 24, 48 hours. PAI-1 mRNA and protein (E) levels were analyzed using real-time RT–PCR and Western blotting, respectively. The RNA and protein levels were normalized to the internal control β-actin. Data are presented as the mean±SEM of three independent experiments. *P < 0.05 vs. corresponding control. **P < 0.01 vs. corresponding control ***P < 0.001 vs. corresponding control.

After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of Quercetin for 3h,followed by 20-minute stimolation of 100ng/ml EGF.

Liver pathology and serum markers of liver injury in mice fed control (Ctrl), or ethanol (EtOH), or ethanol combined with fisetin (E/Fisetin) diet for 4 weeks. (A) Light microscopy with hematoxylin and eosin staining shows lipid accumulation (arrows) in the liver of mice after alcohol exposure, which was alleviated by fisetin administration. (B) Plasma alanine aminotransferase (ALT) and (C) aspartate aminotransferase (AST) activities. Infinity ALT and AST reagents were used formeasuring ALT and AST activities. Scale bar: 50 lm. Results are mean±SD (n = 3 to 6). Results for bars that do not share a letter differed significantly among groups (p < 0.05). Significant differences among groups are determined by analysis of variance followed by Tukey’s test.

After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of Quercetin for 3h,followed by 20-minute stimolation of 100ng/ml EGF.