Journal: Stem Cell Research & Therapy

Article Title: Short-Term DMOG treatment rejuvenates senescent mesenchymal stem cells by enhancing mitochondrial function and mitophagy through the HIF-1α/BNIP3 pathway

doi: 10.1186/s13287-025-04422-2

Figure Lengend Snippet: Short-term DMOG treatment reduces MSC senescence by activating HIF-1α and decreasing apoptosis. ( A , B ) Representative images of SA-β-gal staining showing the proportion of senescent cells in H₂O₂-treated MSCs before and after DMOG treatment. Scale bar = 500 μm. ( C ) Western blot analysis of p53 and p21 protein expression during oxidative stress-induced senescence. ( D , E ) SA-β-gal staining in replicative senescence (P15) MSCs, demonstrating the effect of DMOG in reducing senescence markers. Scale bar = 500 μm. ( F ) Western blot analysis of p53 and p21 protein levels in P5 (young) and P15 (senescent) MSCs. ( G ) Expression levels of senescence-associated genes (IL6, CXCL1, and MMP3) in both senescence models as assessed by qRT-PCR. ( H ) Western blotting and qPCR analysis showing increased HIF-1α protein and mRNA levels in both senescence models after DMOG treatment. ( I ) Calcein/PI live-dead staining revealed an increase in the proportion of live cells following DMOG treatment in both senescence models. ( J , K ) Flow cytometric analysis of apoptosis. Error bars represent the mean ± SD of three independent experiments. Statistical significance was set as p < 0.05. Full-length blots are presented in Supplementary Materials - WB Raw Data

Article Snippet: The primary antibodies used were p53 (1:1000, BM4309, Boster, China), p21 (1:1000, BM3990, Boster, China), HIF-1α (1:1000, BM4083, Boster, China), MFN1 (1:1000, BM4882, Boster, China), MFN2 (1:1000, BM4906, Boster, China), FIS1 (1:1000, A01932-3, Boster, China), BNIP3 (1:1000, BA4304-2, Boster, China), and GAPDH (1:5000, BM1632, Boster, China) as an internal control.

Techniques: Staining, Western Blot, Expressing, Quantitative RT-PCR

Journal: Nutrients

Article Title: Dihydromyricetin May Attenuate Skin Aging as a RAGE Inhibitor

doi: 10.3390/nu17111862

Figure Lengend Snippet: DHM delayed cellular senescence induced by AGEs in HFF-1 cells. ( a ) Representative confocal images of SAHF treated with various concentrations of DHM and 200 μg/mL AGEs, scale = 40 μm; ( b ) Quantification of fluorescence intensity of SAHF ( n = 4); ( c ) Representative image of senescence-associated β-galactosidase (SA-β-Gal) staining in cells (100×) treated with 50 μM DHM and/or 200 μg/mL AGEs, with blue-stained cells (indicated by dark arrows) representing SA-β-Gal-positive cells; ( d ) Quantification of the percentage of SA-β-Gal-positive cells ( n = 6); mRNA expression levels of ( e ) CDKN1A and ( f ) CDKN2A following treatment with 50 μM DHM and 200 μg/mL AGEs ( n = 3); ( g ) Representative Western blot showing p21 expression in treated cells. Data are presented as mean ± SEM. $ p < 0.05 vs. AGEs; & p < 0.05 vs. SC. Abbreviation for groups: SC, cells cultured with complete medium containing 0.025% DMSO; AGEs group, cells treated with 200 μg/mL AGEs; DHM, cells treated with 50 μM DHM; DHM + AGEs, cells treated with 50 μM DHM and 200 μg/mL AGEs.

Article Snippet: Then, the blocked PVDF membranes were incubated overnight at 4 °C with rabbit monoclonal antibodies against p21 Waf1/Cip1 (1:1000, #2947, Cell Signaling Technology, Danvers, MA, USA) or β-actin (1:1000, #4970, Cell Signaling Technology, Danvers, MA, USA).

Techniques: Fluorescence, Staining, Expressing, Western Blot, Cell Culture