SIRT1 Antibody - #BF0189

Fig. 3. The SIRT 1 expression levels and cytoplasmic translocation of HMGB 1. A Immunofluorescence co-location results of SIRT 1 (× 400). B Immunofluorescence co-localization results of HMGB 1 (× 400). Red arrow: overlap between PECAM-1 and HMGB 1. C-F The expression levels of cytoplasmic and nuclear HMGB 1 were determined by Western blot. The protein bands of nuclear HMGB 1 (C), the average optical density value of nuclear HMGB 1 (D), The protein bands of cytoplasmic HMGB 1 (E), the average optical density value of cytoplasmic HMGB 1 (F). G-I Serum SIRT 1, HMGB 1 and Ac-HMGB 1 levels were detected by ELISA. Level of serum SIRT 1 (G), level of serum HMGB 1 (H), level of serum Ac-HMGB 1 (I). J-L Renal Ac-HMGB 1 and SIRT 1 levels were detected by western blot. The protein bands of SIRT 1 and Ac-HMGB 1 (J), the average optical density value of SIRT 1 (K), the average optical density value of Ac-HMGB 1 (L). * p 

Figure 6 ｜ Intranasal insulin administration alters cognitive dysfunction and activates insulin signaling. (A) Schematic diagram of the experimental schedule. After 8 weeks of diabetes, diabetic rats were treated with insulin or vehicle for 6 weeks, and rat behaviors were investigated by the MWM (n = 15 per group). (B–E) Learning functions were evaluated by the escape latency time over 4 days (B). The latency time on days 2 (C), 3 (D), and 4 (E) were analyzed. (F–H) The memory functions of rats were assessed by the time spent in the target quadrant (F), the number of times that the rats crossed the expected platform location (G), and the percentage of distance in the target quadrant (H). (I–L) Protein expression levels were examined (n = 6 per group). Insulin administration increased the expression of p-IR (optical density ratio to IR) (J), p-IRS-1 (optical density ratio to IRS-1) (K), and SIRT1 (optical density ratio to GAPDH) (L) in the hippocampus of diabetic rats with cognitive decline. Data are presented as the mean ± SEM. *P < 0.05, **P < 0.01 (one-way analysis of variance). The experiments were repeated 3 times. DIA: Diabetic rats; GAPDH: glyceraldehyde- 3-phosphate dehydrogenase; IR: insulin receptor; IRS-1: IR receptor substrate 1; MWM: Morris water maze test; NS: non-streptozotocin rats; p-IR: phospho-insulin receptor; p-IRS-1: phospho-insulin receptor substrate; SIRT1: Sirtuin 1.

Figure 8. Low expression of ADRB2, SIRT1, PGC-1α, and PPARα in ethanol-induced alcoholic hepatitis. (A) Western blot analysis of ADRB2 in NIAAA mouse liver tissues. (B) Statistical results of NIAAA mouse liver western blot analysis. (C) Immunofluorescence of ADRB2 and SIRT1 in NIAAA mouse liver tissue. (D) Western blot analysis of ADRB2, PPARα, PGC-1α, and SIRT1 in ALD mouse liver tissues. (E) Statistical results of ALD mouse liver western blot analysis. (F) Immunofluorescence of ADRB2 and SIRT1 in ALD mouse liver tissue. * Represents p < 0.05 and ** represents p < 0.01, compared with the control group.

Figure 8. Low expression of ADRB2, SIRT1, PGC-1α, and PPARα in ethanol-induced alcoholic hepatitis. (A) Western blot analysis of ADRB2 in NIAAA mouse liver tissues. (B) Statistical results of NIAAA mouse liver western blot analysis. (C) Immunofluorescence of ADRB2 and SIRT1 in NIAAA mouse liver tissue. (D) Western blot analysis of ADRB2, PPARα, PGC-1α, and SIRT1 in ALD mouse liver tissues. (E) Statistical results of ALD mouse liver western blot analysis. (F) Immunofluorescence of ADRB2 and SIRT1 in ALD mouse liver tissue. * Represents p < 0.05 and ** represents p < 0.01, compared with the control group.

Fig. 1. The expression of Sirt1 involved in lipid accumulation in HG-induced HepG2 cells. (A) The effects of glucose concentration (25, 30, 35, 40, 45, 50, 55, 60, 70, 80 and 90 mM) on viability of HepG2 cells by MTT. (B) The effects of induced time (0, 12, 24, 48, 72 and 96 h) exposed to 60 mM glucose on the viability of HepG2 cells by MTT. (C) The TG and T-CHO levels in HepG2 cells exposed to 25 mM, 45 mM and 60 mM glucose for 48 h. (D) The TG and T-CHO levels in HepG2 cells exposed to 60 mM glucose for 0 h, 24 h and 48 h. (E) Oil Red O staining in different groups of HepG2 cells. (F, G) The relative protein levels and distribution of Sirt1 in HepG2 cells exposed to 25 mM, 45 mM and 60 mM glucose for 48 h. (H, I) The relative protein levels and distribution of Sirt1 in HepG2 cells exposed to 60 mM glucose for 0 h, 24 h and 48 h. Each bar represents the mean ± SEM for groups of three. *P < 0.05, **P < 0.01, compared to 0 h or 25 mM as indicated.

Fig. 1. The expression of Sirt1 involved in lipid accumulation in HG-induced HepG2 cells. (A) The effects of glucose concentration (25, 30, 35, 40, 45, 50, 55, 60, 70, 80 and 90 mM) on viability of HepG2 cells by MTT. (B) The effects of induced time (0, 12, 24, 48, 72 and 96 h) exposed to 60 mM glucose on the viability of HepG2 cells by MTT. (C) The TG and T-CHO levels in HepG2 cells exposed to 25 mM, 45 mM and 60 mM glucose for 48 h. (D) The TG and T-CHO levels in HepG2 cells exposed to 60 mM glucose for 0 h, 24 h and 48 h. (E) Oil Red O staining in different groups of HepG2 cells. (F, G) The relative protein levels and distribution of Sirt1 in HepG2 cells exposed to 25 mM, 45 mM and 60 mM glucose for 48 h. (H, I) The relative protein levels and distribution of Sirt1 in HepG2 cells exposed to 60 mM glucose for 0 h, 24 h and 48 h. Each bar represents the mean ± SEM for groups of three. *P < 0.05, **P < 0.01, compared to 0 h or 25 mM as indicated.

Fig. 7. Effect of THSWD on SIRT1/FOXO1 pathway in MCAO/R rats and OGD/R PC12 cells (A) SIRT1/FOXO1 pathway protein expression in MCAO/R rats; (B-D) Expression of SIRT1, FOXO1 and Ac-FOXO1 proteins in MCAO/R rats; (E) Protein expression of SIRT1/FOXO1 pathway in OGD/R PC12 cells; (F-H) Expression of SIRT1, FOXO1 and Ac-FOXO1 proteins in OGD/R PC12 cells. (n = 3, #P < 0.05 vs Sham; ##P < 0.01 vs Sham or Control; *P < 0.05 vs Model or OGD/R; **P < 0.01 vs Model or OGD/R).