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New Brunswick Scientific purified high-fat diet hf
Purified High Fat Diet Hf, supplied by New Brunswick Scientific, 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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Purification:

Article Title: Metabolic and transcriptional effects of bazedoxifene/conjugated estrogens in a model of obesity-associated breast cancer risk.
Article Snippet: Rats were also given ad libitum access to a purified high-fat diet (HF; 46% kcal from fat; Research Diets #D12344, New Brunswick, NJ) to induce obesity in this genetically susceptible strain (53-56).

Article Title: Supplementation with Nicotinamide Riboside Reduces Brain Inflammation and Improves Cognitive Function in Diabetic Mice
Article Snippet: After one week of adaption to the laboratory conditions, ICR mice were placed with either standard chow diet (control; 10% kcal fat, D12450B, Research diet, New Brunswick, NJ, USA) or high-fat chow diet (HF; 60% kcal fat, D12492).

Article Title: The prolonged survival of fibroblasts with forced lipid catabolism in visceral fat following encapsulation in alginate-poly-L-lysine
Article Snippet: Four (4 weeks old) C57BL/6J (WT) and six Aldh1a1 −/− female mice were fed a high-fat diet (HF, 45% kcal from fat with standard vitamin A content, 4 IU/g, {"type":"entrez-nucleotide","attrs":{"text":"D12451","term_id":"767753","term_text":"D12451"}} D12451 , Research Diets Inc., New Brunswick, NJ) for 14 months.

Article Title: Programmed Hyperphagia in Offspring of Obese Dams: Altered Expression of Hypothalamic Nutrient Sensors, Neurogenic Factors and Epigenetic Modulators
Article Snippet: Beginning as weanlings, female rats were fed a high fat (HF; 60% kcal fat, Research Purified Diet 1249258Y1, New Brunswick, NJ; N=6) or Control (10% kcal fat, Research Purified Diet 12450B58Y2, New Brunswick, NJ; N=6) diet.

Article Title: Overproduction of Angiotensinogen from adipose Tissue Induces adipose Infammation, Glucose Intolerance, and Insulin Resistance
Article Snippet: For the second study, a separate cohort of male mice were fed a high-fat (HF) diet (45, 20, and 35% of energy from fat, protein, and carbohydrate, respectively; {"type":"entrez-nucleotide","attrs":{"text":"D12451","term_id":"767753","term_text":"D12451"}} D12451 ; Research Diets, New Brunswick, NJ) ( 19 ) for 12 weeks from the time of weaning.

Article Title: Genetic architecture of heart mitochondrial proteome influencing cardiac hypertrophy
Article Snippet: For DIO model, mice were fed ad libitum a chow diet (Ralston Purina Company) until 8 weeks of age and then placed ad libitum on a high-fat/high-sucrose (HF/HS) diet (Research Diets-D12266B, New Brunswick, NJ) with 16.8% kcal protein, 51.4% kcal carbohydrate, 31.8% kcal fat for an additional 8 weeks.

Article Title: Maternal High-Fat-Diet Programs Rat Offspring Liver Fatty Acid Metabolism
Article Snippet: The rats were randomly assigned to either a diet high in fat (HF 60 % kcal fat, 20 % kcal protein, 20 % kcal carbohydrate, purified diet 58Y1, New Brunswick, NJ, USA; n = 5–6) to induce obesity or a normal control diet (control 10 % kcal fat, 20 % kcal protein, 70 % kcal carbohydrate, purified diet 58Y2; n = 5–6).

Article Title: Mesenchymal Stem Cells Shift Mitochondrial Dynamics and Enhance Oxidative Phosphorylation in Recipient Cells.
Article Snippet: At 4 weeks of age, animals were placed on a high-fat diet (HF, 60% kcal fat; D12492, ResearchDiets; NewBrunswick, NJ) for 20 weeks in order to elicit metabolic inflammation (Guo et al., 2009).

Control:

Article Title: Metabolic and transcriptional effects of bazedoxifene/conjugated estrogens in a model of obesity-associated breast cancer risk.
Article Snippet: Rats were also given ad libitum access to a purified high-fat diet (HF; 46% kcal from fat; Research Diets #D12344, New Brunswick, NJ) to induce obesity in this genetically susceptible strain (53-56).

Article Title: Supplementation with Nicotinamide Riboside Reduces Brain Inflammation and Improves Cognitive Function in Diabetic Mice
Article Snippet: After one week of adaption to the laboratory conditions, ICR mice were placed with either standard chow diet (control; 10% kcal fat, D12450B, Research diet, New Brunswick, NJ, USA) or high-fat chow diet (HF; 60% kcal fat, D12492).

Article Title: The prolonged survival of fibroblasts with forced lipid catabolism in visceral fat following encapsulation in alginate-poly-L-lysine
Article Snippet: Four (4 weeks old) C57BL/6J (WT) and six Aldh1a1 −/− female mice were fed a high-fat diet (HF, 45% kcal from fat with standard vitamin A content, 4 IU/g, {"type":"entrez-nucleotide","attrs":{"text":"D12451","term_id":"767753","term_text":"D12451"}} D12451 , Research Diets Inc., New Brunswick, NJ) for 14 months.

Article Title: Programmed Hyperphagia in Offspring of Obese Dams: Altered Expression of Hypothalamic Nutrient Sensors, Neurogenic Factors and Epigenetic Modulators
Article Snippet: Beginning as weanlings, female rats were fed a high fat (HF; 60% kcal fat, Research Purified Diet 1249258Y1, New Brunswick, NJ; N=6) or Control (10% kcal fat, Research Purified Diet 12450B58Y2, New Brunswick, NJ; N=6) diet.

Article Title: Overproduction of Angiotensinogen from adipose Tissue Induces adipose Infammation, Glucose Intolerance, and Insulin Resistance
Article Snippet: For the second study, a separate cohort of male mice were fed a high-fat (HF) diet (45, 20, and 35% of energy from fat, protein, and carbohydrate, respectively; {"type":"entrez-nucleotide","attrs":{"text":"D12451","term_id":"767753","term_text":"D12451"}} D12451 ; Research Diets, New Brunswick, NJ) ( 19 ) for 12 weeks from the time of weaning.

Article Title: Genetic architecture of heart mitochondrial proteome influencing cardiac hypertrophy
Article Snippet: For DIO model, mice were fed ad libitum a chow diet (Ralston Purina Company) until 8 weeks of age and then placed ad libitum on a high-fat/high-sucrose (HF/HS) diet (Research Diets-D12266B, New Brunswick, NJ) with 16.8% kcal protein, 51.4% kcal carbohydrate, 31.8% kcal fat for an additional 8 weeks.

Article Title: Maternal High-Fat-Diet Programs Rat Offspring Liver Fatty Acid Metabolism
Article Snippet: The rats were randomly assigned to either a diet high in fat (HF 60 % kcal fat, 20 % kcal protein, 20 % kcal carbohydrate, purified diet 58Y1, New Brunswick, NJ, USA; n = 5–6) to induce obesity or a normal control diet (control 10 % kcal fat, 20 % kcal protein, 70 % kcal carbohydrate, purified diet 58Y2; n = 5–6).

Article Title: Mesenchymal Stem Cells Shift Mitochondrial Dynamics and Enhance Oxidative Phosphorylation in Recipient Cells.
Article Snippet: At 4 weeks of age, animals were placed on a high-fat diet (HF, 60% kcal fat; D12492, ResearchDiets; NewBrunswick, NJ) for 20 weeks in order to elicit metabolic inflammation (Guo et al., 2009).



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STING activation is required for TGF-β-mediated upregulation of HSC transdifferentiation genes. (A) Representative images of mouse primary HSC immunostained for p-STING (green) and expressing Golgi-RFP (CellLight Golgi-RFP—red). Pretreatment with 10 μM STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of STING and its localization in Golgi. (B) STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of IRF3 (green) and its nuclear colocalization in mouse primary ? HSC. α-SMA expression has been shown to indicate activated status of HSCs. (C) STING inhibitor (STING-X) blocks TGF-β-mediated activation of an ACTA2 reporter (green signal) (data represented as mean ± SD; n = 6 biologically independent samples for (A) and (B) and n = 10 biologically independent samples for (C), 1-way ANOVA, ****p < 0.0001) (D) STING inhibitor (STING-X) limits the upregulation (ECM inflammatory, ECM remodeling, differentiation, and ECM deposition) and downregulation (ECM remodeling) of a wide range of functionally significant transcriptional signals mediated by TGF-β (n = 4 biologically independent samples per each group). (E) STING inhibitor blocks phosphorylation of STING and IRF3 and upregulation of α-SMA. Immunoblot image is representative of three independent experiments. (F) C57BL/6N mice were subjected to CCl4 (0.5 mL/kg b.wt. i.p) 3 times a week for 4 weeks followed by STING inhibitor (CCl4 + STINGX) (20 mg/kg b.wt. i.p) 3 times a week for following 4 week alongside CCl4 injections (total 8 weeks). STING-X reverses the fibrosis induced by CCl4 toxicity as demonstrated by significant reduction of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×10objective field quantified; Data analyzed by Student t test) (**p < 0.01). (G) STING inhibitor (STING-X) blocks <t>high-fat</t> <t>choline-deficient</t> <t>amino</t> <t>acid-supplemented</t> (HF-CDAA) diet-induced liver fibrosis in C57BL/6N mice as demonstrated by lack of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×20 objective field quantified; data analyzed by Student t test). Abbreviations: α-SMA, alpha-smooth muscle actin; ECM, extracellular matrix; STING, stimulator of interferon genes.
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STING activation is required for TGF-β-mediated upregulation of HSC transdifferentiation genes. (A) Representative images of mouse primary HSC immunostained for p-STING (green) and expressing Golgi-RFP (CellLight Golgi-RFP—red). Pretreatment with 10 μM STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of STING and its localization in Golgi. (B) STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of IRF3 (green) and its nuclear colocalization in mouse primary ? HSC. α-SMA expression has been shown to indicate activated status of HSCs. (C) STING inhibitor (STING-X) blocks TGF-β-mediated activation of an ACTA2 reporter (green signal) (data represented as mean ± SD; n = 6 biologically independent samples for (A) and (B) and n = 10 biologically independent samples for (C), 1-way ANOVA, ****p < 0.0001) (D) STING inhibitor (STING-X) limits the upregulation (ECM inflammatory, ECM remodeling, differentiation, and ECM deposition) and downregulation (ECM remodeling) of a wide range of functionally significant transcriptional signals mediated by TGF-β (n = 4 biologically independent samples per each group). (E) STING inhibitor blocks phosphorylation of STING and IRF3 and upregulation of α-SMA. Immunoblot image is representative of three independent experiments. (F) C57BL/6N mice were subjected to CCl4 (0.5 mL/kg b.wt. i.p) 3 times a week for 4 weeks followed by STING inhibitor (CCl4 + STINGX) (20 mg/kg b.wt. i.p) 3 times a week for following 4 week alongside CCl4 injections (total 8 weeks). STING-X reverses the fibrosis induced by CCl4 toxicity as demonstrated by significant reduction of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×10objective field quantified; Data analyzed by Student t test) (**p < 0.01). (G) STING inhibitor (STING-X) blocks <t>high-fat</t> <t>choline-deficient</t> <t>amino</t> <t>acid-supplemented</t> (HF-CDAA) diet-induced liver fibrosis in C57BL/6N mice as demonstrated by lack of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×20 objective field quantified; data analyzed by Student t test). Abbreviations: α-SMA, alpha-smooth muscle actin; ECM, extracellular matrix; STING, stimulator of interferon genes.
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STING activation is required for TGF-β-mediated upregulation of HSC transdifferentiation genes. (A) Representative images of mouse primary HSC immunostained for p-STING (green) and expressing Golgi-RFP (CellLight Golgi-RFP—red). Pretreatment with 10 μM STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of STING and its localization in Golgi. (B) STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of IRF3 (green) and its nuclear colocalization in mouse primary ? HSC. α-SMA expression has been shown to indicate activated status of HSCs. (C) STING inhibitor (STING-X) blocks TGF-β-mediated activation of an ACTA2 reporter (green signal) (data represented as mean ± SD; n = 6 biologically independent samples for (A) and (B) and n = 10 biologically independent samples for (C), 1-way ANOVA, ****p < 0.0001) (D) STING inhibitor (STING-X) limits the upregulation (ECM inflammatory, ECM remodeling, differentiation, and ECM deposition) and downregulation (ECM remodeling) of a wide range of functionally significant transcriptional signals mediated by TGF-β (n = 4 biologically independent samples per each group). (E) STING inhibitor blocks phosphorylation of STING and IRF3 and upregulation of α-SMA. Immunoblot image is representative of three independent experiments. (F) C57BL/6N mice were subjected to CCl4 (0.5 mL/kg b.wt. i.p) 3 times a week for 4 weeks followed by STING inhibitor (CCl4 + STINGX) (20 mg/kg b.wt. i.p) 3 times a week for following 4 week alongside CCl4 injections (total 8 weeks). STING-X reverses the fibrosis induced by CCl4 toxicity as demonstrated by significant reduction of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×10objective field quantified; Data analyzed by Student t test) (**p < 0.01). (G) STING inhibitor (STING-X) blocks <t>high-fat</t> <t>choline-deficient</t> <t>amino</t> <t>acid-supplemented</t> (HF-CDAA) diet-induced liver fibrosis in C57BL/6N mice as demonstrated by lack of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×20 objective field quantified; data analyzed by Student t test). Abbreviations: α-SMA, alpha-smooth muscle actin; ECM, extracellular matrix; STING, stimulator of interferon genes.
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Image Search Results


STING activation is required for TGF-β-mediated upregulation of HSC transdifferentiation genes. (A) Representative images of mouse primary HSC immunostained for p-STING (green) and expressing Golgi-RFP (CellLight Golgi-RFP—red). Pretreatment with 10 μM STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of STING and its localization in Golgi. (B) STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of IRF3 (green) and its nuclear colocalization in mouse primary ? HSC. α-SMA expression has been shown to indicate activated status of HSCs. (C) STING inhibitor (STING-X) blocks TGF-β-mediated activation of an ACTA2 reporter (green signal) (data represented as mean ± SD; n = 6 biologically independent samples for (A) and (B) and n = 10 biologically independent samples for (C), 1-way ANOVA, ****p < 0.0001) (D) STING inhibitor (STING-X) limits the upregulation (ECM inflammatory, ECM remodeling, differentiation, and ECM deposition) and downregulation (ECM remodeling) of a wide range of functionally significant transcriptional signals mediated by TGF-β (n = 4 biologically independent samples per each group). (E) STING inhibitor blocks phosphorylation of STING and IRF3 and upregulation of α-SMA. Immunoblot image is representative of three independent experiments. (F) C57BL/6N mice were subjected to CCl4 (0.5 mL/kg b.wt. i.p) 3 times a week for 4 weeks followed by STING inhibitor (CCl4 + STINGX) (20 mg/kg b.wt. i.p) 3 times a week for following 4 week alongside CCl4 injections (total 8 weeks). STING-X reverses the fibrosis induced by CCl4 toxicity as demonstrated by significant reduction of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×10objective field quantified; Data analyzed by Student t test) (**p < 0.01). (G) STING inhibitor (STING-X) blocks high-fat choline-deficient amino acid-supplemented (HF-CDAA) diet-induced liver fibrosis in C57BL/6N mice as demonstrated by lack of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×20 objective field quantified; data analyzed by Student t test). Abbreviations: α-SMA, alpha-smooth muscle actin; ECM, extracellular matrix; STING, stimulator of interferon genes.

Journal: Hepatology (Baltimore, Md.)

Article Title: Mitochondrial DNA and the STING pathway are required for hepatic stellate cell activation

doi: 10.1097/HEP.0000000000000388

Figure Lengend Snippet: STING activation is required for TGF-β-mediated upregulation of HSC transdifferentiation genes. (A) Representative images of mouse primary HSC immunostained for p-STING (green) and expressing Golgi-RFP (CellLight Golgi-RFP—red). Pretreatment with 10 μM STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of STING and its localization in Golgi. (B) STING inhibitor (STING-X) blocks TGF-β-mediated phosphorylation of IRF3 (green) and its nuclear colocalization in mouse primary ? HSC. α-SMA expression has been shown to indicate activated status of HSCs. (C) STING inhibitor (STING-X) blocks TGF-β-mediated activation of an ACTA2 reporter (green signal) (data represented as mean ± SD; n = 6 biologically independent samples for (A) and (B) and n = 10 biologically independent samples for (C), 1-way ANOVA, ****p < 0.0001) (D) STING inhibitor (STING-X) limits the upregulation (ECM inflammatory, ECM remodeling, differentiation, and ECM deposition) and downregulation (ECM remodeling) of a wide range of functionally significant transcriptional signals mediated by TGF-β (n = 4 biologically independent samples per each group). (E) STING inhibitor blocks phosphorylation of STING and IRF3 and upregulation of α-SMA. Immunoblot image is representative of three independent experiments. (F) C57BL/6N mice were subjected to CCl4 (0.5 mL/kg b.wt. i.p) 3 times a week for 4 weeks followed by STING inhibitor (CCl4 + STINGX) (20 mg/kg b.wt. i.p) 3 times a week for following 4 week alongside CCl4 injections (total 8 weeks). STING-X reverses the fibrosis induced by CCl4 toxicity as demonstrated by significant reduction of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×10objective field quantified; Data analyzed by Student t test) (**p < 0.01). (G) STING inhibitor (STING-X) blocks high-fat choline-deficient amino acid-supplemented (HF-CDAA) diet-induced liver fibrosis in C57BL/6N mice as demonstrated by lack of Sirius Red staining (data shown as mean ± SD; n = 8 mice per each group, each data point in the graph plot represents individual ×20 objective field quantified; data analyzed by Student t test). Abbreviations: α-SMA, alpha-smooth muscle actin; ECM, extracellular matrix; STING, stimulator of interferon genes.

Article Snippet: C57BL/6N mice were subjected to high-fat choline-deficient amino acid-supplemented (HF-CDAA) diet (A06071302), l -amino acid diet with 60% kcal % fat with 0.1% methionine, and no added choline (Research diets Inc., USA) for 6 weeks.

Techniques: Activation Assay, Expressing, Western Blot, Staining