Journal: The Journal of Physiological Sciences : JPS

Article Title: SIRT3-dependent enhancement of apelinergic signaling mediates the cardioprotective effects of late-life high-intensity interval training

doi: 10.1016/j.jphyss.2026.100061

Figure Lengend Snippet: SIRT3 mediated the protective role of apelinergic signaling in senescent cardiomyocytes Bubble chart showing comparing enrichment of mitochondrium-related pathways between HIIT-NC versus HIIT-shAPJ by GSEA analysis. X-axis: normalized enrichment score of GSEA analysis. Y-axis: mitochondrium-related enrichment pathways. The color of the bubble refers to the enrichment p -value with −log10 for visualization, and the size of the bubble refers to the number of DEGs in corresponding pathway. Mito, mitochondrial. (B) Rank-based gene set enrichment analysis of genes significantly more modulated by mitochondrium-related pathways preferentially induced by HIIT-NC compared to HIIT-shAPJ. NES, normalized enriching scores. (C) Expression and quantification of SIRT3 proteins in the left ventricle among CON-NC, HIIT-NC and HIIT-shAPJ detected by WB (n = 5). (D) Expression and quantification of SIRT3 proteins of AC16 cell pretreated with FBS and Apelin-13 (10 −9 -10 −5 mmol/L, 30 min), then treatment of D -gal (20 g/L, 48 hr) detected by WB (n = 3). (E) Expression and quantification of SIRT3 proteins of senescent AC16 cell pretreated with shSIRT3 or shRNA scramble transfection, subsequent FBS or Apelin-13 detected by WB (n = 4). (F) mRNA expression of p16 in senescent AC16 cell pretreated with shSIRT3 or shRNA sceamble transfection, subsequent FBS or Apelin-13 (n = 4). (G) Representative images of AC16 cell with senescence β-galactosidase staining with or without shSIRT3 and Apelin. (H) Representative images of immunofluorescence with JC-1 probe to detect mitochondrial membrane potential. (I) Quantification of AC16 cell with senescence β-galactosidase staining with or without shSIRT3 and Apelin (n = 4). (J) Quantification of immunofluorescence with JC-1 probe to detect mitochondrial membrane potential (n = 5). (K) Representative images of mitochondrial morphology by TEM in × 2000, × 8000 and × 20000 magnification (ER, endoplasmic reticulum; G, Golgi apparatus; Ly, lysosome; M, mitochondria; N, nucleus). (L) Analysis of mitochondrial respiration of senescent AC16 cells using the Seahorse platform (n = 5). Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The mitochondrial membrane potential was measured following the instructions of a JC-1 detection kit (Beyotime Biotechnology, China).

Techniques: Expressing, shRNA, Transfection, Staining, Immunofluorescence, Membrane

Journal: The FASEB Journal

Article Title: The role of chemerin in the regulation of cGAS‐STING pathway in gestational diabetes mellitus placenta

doi: 10.1096/fj.202201611r

Figure Lengend Snippet: FIGURE 1 The differences of placental morphology and mitochondrial structure in GDM patients and normal pregnant women. (A) Representative TEM image of GDM placenta mitochondria (scale bar = 500 nm). (B) Representative TEM image of placenta mitochondria in the control group (scale bar = 500 nm). (C) Specific surface of mitochondria analysis. (D) Representative image of HE staining in GDM placenta (scale bar = 100 μm). (E) Representative image of HE staining in placenta of the control group (scale bar = 100 μm). White arrows indicated placental mitochondria. GDM: gestational diabetes mellitus; TEM: transmission electron microscope; HE: hematoxylin eosin. Data were shown as mean ± SD (n ≥ 3). *p < .05.

Article Snippet: 3.7 | The mitochondrial membrane potential was diminished and phosphorylation of TBK1 and IRF3 protein were enhanced in the HTR- 8/ SVneo cell model To confirm the changes of the mitochondrial membrane potential in the HG and IR cell models, JC- 1 assay kit (C2006, Beyotime Biotechnology, China) was used according to the manufacturer's protocol.

Techniques: Control, Staining, Transmission Assay, Microscopy

Journal: Cell Communication and Signaling : CCS

Article Title: Momordicine-I suppresses head and neck cancer growth by modulating key metabolic pathways

doi: 10.1186/s12964-024-01951-w

Figure Lengend Snippet: M-I treatment inhibits glycolysis and lipogenesis in vivo . MOC2 cells (1 × 10 6 ) were injected subcutaneously into C57BL/6 mice. Tumor‐bearing mice were randomly divided into two groups. The control group received vehicle, and the experimental group received 30 mg/kg/mouse M-I via intraperitoneal injection every day until the end of the experiment. A Tumor volume post-M-I treatment. B Representative images of tumors from control and M-I-treated groups. C Relative mRNA expression of Hk1 , Pdk3 , Fasn and Acly was analysed by qRT-PCR from control or M-I treated tumor RNA.18 s gene was used as internal control. Small bar indicates standard error (*, p < 0.05; **, p < 0.01). n = 3 technical replicates

Article Snippet: To measure the lactate production, glycolysis kit (Dojindo Laboratories-G272) was used according to the instruction.

Techniques: In Vivo, Injection, Control, Expressing, Quantitative RT-PCR