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nmol l a1r inhibitor derenofylline  (MedChemExpress)
93
MedChemExpress nmol l a1r inhibitor derenofylline
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
Nmol L A1r Inhibitor Derenofylline, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a1r confocal laser scanning microscope  (Nikon)
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Nikon a1r confocal laser scanning microscope
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
A1r Confocal Laser Scanning Microscope, supplied by Nikon, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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confocal microscope nikon a1r  (Nikon)
90
Nikon confocal microscope nikon a1r
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
Confocal Microscope Nikon A1r, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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confocal laser scanning microscope nikon a1r mp  (Nikon)
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Nikon confocal laser scanning microscope nikon a1r mp
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
Confocal Laser Scanning Microscope Nikon A1r Mp, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a1r confocal microscope  (Nikon)
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Nikon a1r confocal microscope
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
A1r Confocal Microscope, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nikon-a1r confocal microscope  (Nikon)
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Nikon nikon-a1r confocal microscope
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
Nikon A1r Confocal Microscope, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nikon a1r confocal  (Nikon)
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Nikon nikon a1r confocal
Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L <t>SLV320</t> (an <t>adenosine</t> <t>A1</t> <t>receptor</t> inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.
Nikon A1r Confocal, supplied by Nikon, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.

Journal: Animal Nutrition

Article Title: Ruminal microbiota-derived inosine alleviates metabolic disorders in dairy cows supplemented with grape seed extract

doi: 10.1016/j.aninu.2025.04.009

Figure Lengend Snippet: Inosine alleviated lipid accumulation and activated insulin signaling and gluconeogenesis in bovine hepatocytes. (A) Representative image of Nile red staining in hepatocytes (scale bar = 100 μm). Hepatocytes were treated for 12 h with 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B–F) Hepatocytes were treated for 12 h with 1 μmol/L inosine, 1.2 mmol/L NEFA, 1.2 mmol/L NEFA and 1 μmol/L inosine in combination, or untreated (Control). (B-D) Western blotting of SREBP-1c and PPARα in hepatocytes. (E and F) Western blotting of p-AKT/AKT in hepatocytes, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (G) Triglyceride content. Hepatocytes were pre-treated with 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) for 30 min, or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor), and then treated with 1.2 mmol/L NEFA and 1 μmol/L inosine for 12 h. (H–O) Hepatocytes were pre-treated with SCH58261 for 30 min and then treated with NEFA and inosine for 12 h. (H) Representative image of Nile red staining (scale bar = 100 μm). (I–K) Western blot analysis of SREBP-1c and PPARα. (L and M) Western blotting of p-AKT/AKT, cells were treated with 100 nmol/L insulin for 30 min before harvesting. (N and O) Western blotting of p-AKT/AKT. Hepatocytes were treated with 1 μmol/L SLV320 for 30 min or transfected with Si-A2bR or Si-A3R, and then treated with NEFA and inosine for 12 h, and treated with 100 nmol/L insulin for 30 min before harvesting. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). NEFA = non-esterified fatty acid; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; AKT = protein kinase B; p-AKT = phosphorylation of AKT.

Article Snippet: To determine the biologically-active inosine receptor type in hepatocyte metabolism, hepatocytes were separately pretreated with: 1) 100 nmol/L A1R inhibitor derenofylline (SLV320, Cat. # HY-14858, MedChemExpress, Shanghai, China); 2) 1 μmol/L A2aR inhibitor ( SCH58261 , Cat. # HY-19533, MedChemExpress); 3) siRNA against A2bR or A3R.

Techniques: Staining, Control, Western Blot, Transfection, Small Interfering RNA, Binding Assay, Phospho-proteomics

Inosine inhibited lipolysis and inflammation in bovine adipocytes. (A and B) Triglyceride content in adipocytes and glycerol content in the supernatant. Cells were treated with 0, 1, 2, 5 and 10 μmol/L inosine for 12 h after 10 μmol/L ISO pre-treatment for 3 h. (C-E) Western blotting of p-HSL/HSL and ATGL. Adipocytes were treated with 1 μmol/L inosine for 12 h after pre-treatment with ISO for 3 h. (F–H) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with 1 μmol/L inosine, 1 μg/mL LPS or co-treatment for 12 h. (I and J) Triglyceride content in adipocytes and glycerol content in supernatant. Adipocytes were pre-treated with 10 μmol/L ISO for 3 h, and then treated with 1 μmol/L inosine for 12 h after 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) treatment for 30 min or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor). (K-M) Western blotting of p-HSL/HSL and ATGL. Adipocytes were pre-treated with ISO for 3 h, and then treated with inosine for 12 h after SLV320 treatment for 30 min. (N–P) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with inosine and LPS for 12 h, after SLV320 treatment for 30 min. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). ISO = isoprenaline hydrochloride; HSL = hormone-sensitive lipase; p-HSL = phosphorylation of HSL; ATGL = adipose triglyceride lipase; NF-κB = nuclear factor kappa B; p–NF–κB = phosphorylation of NF-κB; IκBα = NF-κB inhibitor alpha; p-IκBα = phosphorylation of IκBα; LPS = lipopolysaccharide.

Journal: Animal Nutrition

Article Title: Ruminal microbiota-derived inosine alleviates metabolic disorders in dairy cows supplemented with grape seed extract

doi: 10.1016/j.aninu.2025.04.009

Figure Lengend Snippet: Inosine inhibited lipolysis and inflammation in bovine adipocytes. (A and B) Triglyceride content in adipocytes and glycerol content in the supernatant. Cells were treated with 0, 1, 2, 5 and 10 μmol/L inosine for 12 h after 10 μmol/L ISO pre-treatment for 3 h. (C-E) Western blotting of p-HSL/HSL and ATGL. Adipocytes were treated with 1 μmol/L inosine for 12 h after pre-treatment with ISO for 3 h. (F–H) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with 1 μmol/L inosine, 1 μg/mL LPS or co-treatment for 12 h. (I and J) Triglyceride content in adipocytes and glycerol content in supernatant. Adipocytes were pre-treated with 10 μmol/L ISO for 3 h, and then treated with 1 μmol/L inosine for 12 h after 100 nmol/L SLV320 (an adenosine A1 receptor inhibitor) or 1 μmol/L SCH58261 (an adenosine A2a receptor inhibitor) treatment for 30 min or transfected with Si-A2bR (small interfering RNA for adenosine A2b receptor) or Si-A3R (small interfering RNA for adenosine A3 receptor). (K-M) Western blotting of p-HSL/HSL and ATGL. Adipocytes were pre-treated with ISO for 3 h, and then treated with inosine for 12 h after SLV320 treatment for 30 min. (N–P) Western blotting of p–NF–κB/NF-κB and p-IκBα/IκBα. Adipocytes were treated with inosine and LPS for 12 h, after SLV320 treatment for 30 min. Data are expressed as means ± SEM. Different letters on bars indicate significant differences ( P < 0.05). ISO = isoprenaline hydrochloride; HSL = hormone-sensitive lipase; p-HSL = phosphorylation of HSL; ATGL = adipose triglyceride lipase; NF-κB = nuclear factor kappa B; p–NF–κB = phosphorylation of NF-κB; IκBα = NF-κB inhibitor alpha; p-IκBα = phosphorylation of IκBα; LPS = lipopolysaccharide.

Article Snippet: To determine the biologically-active inosine receptor type in hepatocyte metabolism, hepatocytes were separately pretreated with: 1) 100 nmol/L A1R inhibitor derenofylline (SLV320, Cat. # HY-14858, MedChemExpress, Shanghai, China); 2) 1 μmol/L A2aR inhibitor ( SCH58261 , Cat. # HY-19533, MedChemExpress); 3) siRNA against A2bR or A3R.

Techniques: Western Blot, Transfection, Small Interfering RNA, Phospho-proteomics

Schematic illustration of the mechanism by which grape seed extract (GSE) regulates energy metabolism in dairy cows through ruminal microbiome. Feeding GSE altered the ruminal microbial community composition, which genera including Succiniclasticum , Schwartzia , and Bifidobacterium were significantly enriched in the GSE group, while genera Acetitomaculum , Succinivibrionaceae UCG-001 and Syntrophococcus were significantly reduced. The enrichment of differential genera induced changes in microbial metabolites, which play a role in metabolic regulation. Among the differential metabolites, inosine was notably increased, entering the bloodstream through the rumen epithelium and exerting functions in the liver and adipose tissues. Mechanically, in hepatocytes, inosine enhanced the insulin sensitivity through adenosine A1 receptor (A1R), activated lipid oxidation and inhibited lipid synthesis through adenosine A2a receptor (A2aR). In adipocytes, inosine suppresses lipolysis and inflammation through the A1R. p-AKT = phosphorylation of protein kinase B; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; p-HSL = phosphorylation of hormone-sensitive lipase; ATGL = adipose triglyceride lipase; p–NF–κB = phosphorylation of nuclear factor kappa B.

Journal: Animal Nutrition

Article Title: Ruminal microbiota-derived inosine alleviates metabolic disorders in dairy cows supplemented with grape seed extract

doi: 10.1016/j.aninu.2025.04.009

Figure Lengend Snippet: Schematic illustration of the mechanism by which grape seed extract (GSE) regulates energy metabolism in dairy cows through ruminal microbiome. Feeding GSE altered the ruminal microbial community composition, which genera including Succiniclasticum , Schwartzia , and Bifidobacterium were significantly enriched in the GSE group, while genera Acetitomaculum , Succinivibrionaceae UCG-001 and Syntrophococcus were significantly reduced. The enrichment of differential genera induced changes in microbial metabolites, which play a role in metabolic regulation. Among the differential metabolites, inosine was notably increased, entering the bloodstream through the rumen epithelium and exerting functions in the liver and adipose tissues. Mechanically, in hepatocytes, inosine enhanced the insulin sensitivity through adenosine A1 receptor (A1R), activated lipid oxidation and inhibited lipid synthesis through adenosine A2a receptor (A2aR). In adipocytes, inosine suppresses lipolysis and inflammation through the A1R. p-AKT = phosphorylation of protein kinase B; SREBP-1c = sterol regulatory element binding protein-1c; PPARα = peroxisome proliferator activated receptor alpha; p-HSL = phosphorylation of hormone-sensitive lipase; ATGL = adipose triglyceride lipase; p–NF–κB = phosphorylation of nuclear factor kappa B.

Article Snippet: To determine the biologically-active inosine receptor type in hepatocyte metabolism, hepatocytes were separately pretreated with: 1) 100 nmol/L A1R inhibitor derenofylline (SLV320, Cat. # HY-14858, MedChemExpress, Shanghai, China); 2) 1 μmol/L A2aR inhibitor ( SCH58261 , Cat. # HY-19533, MedChemExpress); 3) siRNA against A2bR or A3R.

Techniques: Phospho-proteomics, Binding Assay