Journal: Redox Biology

Article Title: Alpha-ketoglutarate accelerates granulocyte-monocyte progenitor differentiation and atherosclerotic plaque inflammation via oxoglutarate receptor 1

doi: 10.1016/j.redox.2026.104134

Figure Lengend Snippet: PNP perturbed redox and mitochondrial homeostasis. ( A–G ) Lineage −/low cells were treated with 0 or 0.1 U/mL PNP for 24 h. NAD expression, NMN expression, ATP level, SOD expression and activity, GPX activity, and catalase activity were measured by ELISA. ( H–J ) In parallel, the cells were harvested and incubated with H2DCFDA for 15 min to study the level of ROS by FACS. (K–P) To assess mitochondrial function, lineage −/low cells were treated with PNP for PBS or 24 h. After harvest, 3 × 10 5 cells were loaded for oxygen consumption using a Seahorse Bioscience XF96 extracellular flux analyzer. Two experimental groups were compared using the unpaired two-tailed Student's t-test. In the experiments involving ≥3 groups, one-way analysis of variance followed by Dunnett's test was used.

Article Snippet: Protein was extracted from PNP-treated lineage −/low cells to determine the expression of ribose-5-phosphate, IMPDH2, NAD, SOD, and ATP by ELISA, following the manufacturer's instructions (mouse IMPDH2 ELISA kit [#ml601123], mouse NAD ELISA kit [# JK691233 ], Enzyme-linked Biotechnology, China; mouse SOD ELISA kit [#CSB- E08556 m], Huamei Bioengineering, China; ATP Assay Kit [#HY-K0314], MedChemExpress, US).

Techniques: Expressing, Activity Assay, Enzyme-linked Immunosorbent Assay, Incubation, Two Tailed Test

Journal: Redox Biology

Article Title: Alpha-ketoglutarate accelerates granulocyte-monocyte progenitor differentiation and atherosclerotic plaque inflammation via oxoglutarate receptor 1

doi: 10.1016/j.redox.2026.104134

Figure Lengend Snippet: Correlation of LDL-c and TCA metabolites in human plasma samples. (A-B) The fasting plasma levels of LDL-c and isocitrate were determined in healthy human subjects (n = 40) and their correlation was analyzed by Spearman's correlation analysis. ATP: adenosine triphosphate; ELISA: enzyme-linked immunosorbent assay; GPX: glutathione peroxidase; LDL-c: low-density lipoprotein cholesterol; NAD: nicotinamide adenine dinucleotide; PNP: purine nucleoside phosphorylase; ROS: reactive oxygen species; SOD: superoxide dismutase. (C) A proposed model of HFD-induced skewed myelopoiesis and atherosclerosis via α-ketoglutarate. In mice fed a HFD, isocitrate was elevated and LDL-c increased isocitrate dehydrogenase expression, leading to enhanced α-ketoglutarate production. Acting through OXGR1, α-ketoglutarate upregulated PNP mRNA and protein expression. PNP catabolized guanosine/deoxyguanosine and inosine/deoxyinosine, generating ribose-1-phosphate. By interconversion, ribose-5-phosphate production was increased and initiated de novo purine biosynthesis, resulting in IMPDH2 production and GMP proliferation. PNP metabolized nicotinamide riboside to Nam, decreasing NMN and NAD production. PNP increased NAD kinase expression to further accelerate NAD consumption. Furthermore, PNP increased inflammatory protein expression such as NF-κB. All of which reduced NAD production promoted ROS production and inflammation to facilitate GMP differentiation. Ultimately, the pronounced GMP proliferation and differentiation led to inflammatory myeloid cell production and atherosclerotic progression. GMP: granulocyte-monocyte progenitor; HFD: high-fat diet; IMPDH2: inosine-5′-monophosphate dehydrogenase 2; LDL-c: low-density lipoprotein cholesterol; NAD: nicotinamide adenine dinucleotide; OXGR1: oxoglutarate receptor 1; PNP: purine nucleoside phosphorylase; ROS: reactive oxygen species.

Article Snippet: Protein was extracted from PNP-treated lineage −/low cells to determine the expression of ribose-5-phosphate, IMPDH2, NAD, SOD, and ATP by ELISA, following the manufacturer's instructions (mouse IMPDH2 ELISA kit [#ml601123], mouse NAD ELISA kit [# JK691233 ], Enzyme-linked Biotechnology, China; mouse SOD ELISA kit [#CSB- E08556 m], Huamei Bioengineering, China; ATP Assay Kit [#HY-K0314], MedChemExpress, US).

Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Expressing

Journal: Poultry Science

Article Title: Natural astaxanthin enhances testosterone synthesis by improving mitochondrial function and reducing oxidative stress in Leydig cells

doi: 10.1016/j.psj.2026.106663

Figure Lengend Snippet: Effects of ASTA on MMP, ATP content, relative mtDNA Copy Number and mitochondrial biogenesis-related proteins in rooster Leydig cells. (A) Flow cytometry analysis of mitochondrial membrane potential. (B) Quantification of MMP (% of JC-1 red fluorescence). (C) ATP content in Leydig cells. (D) Relative mtDNA Copy Number. The relative mRNA levels of PGC-1α (E), NRF1 (F), TFAM (G). The relative protein levels of PGC-1α(H, I), NRF1(H, J), TFAM(H, K). The data represent the mean ± SEM; n = 3 in each group. * P < 0.05; ** P < 0.01.

Article Snippet: MMP, cellular ATP levels, and apoptosis in Leydig cells were assessed using the following commercial kits: the JC-1 Mitochondrial Membrane Potential Assay Kit (BiYunTian, China), the ATP Content Assay Kit (Nanjing Jiancheng Bioengineering Institute, China), TIANamp Genomic DNA Kit (Tiangen, Beijing, China) and the Annexin V-FITC Apoptosis Detection Kit (BiYunTian, China), in conjunction with a flow cytometer.

Techniques: Flow Cytometry, Membrane, Fluorescence