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methionine- choline-deficient (mcd) diet  (research diets inc)
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Pharmacological enhancement of ATG16L1 expression prevents MASH development. The protein expression levels of STING signaling components in activated WT BMDMs treated with CM from PAOA-stimulated hepatocytes with or without the ATG16L1 enhancer peretinoin following DMXAA stimulation. (B) The protein levels of p-JNK, JNK, c-Jun, and c-Fos in activated WT BMDMs treated with CM. (C) The proinflammatory protein expression levels, (D) proinflammatory gene expression levels, and (E) Ifnb1 and (F) Tgfb1 mRNA expression in activated WT BMDMs treated with CM. (G) Schematic representation of HFHCD-fed or <t>MCD-fed</t> WT mice supplemented with dietary peretinoin. (H) Hepatic ATG16L1 protein expression levels. (I) Hepatic H&E staining, oil red O staining, Sirius red staining, and α-SMA immunohistochemistry. (J) NAS, serum ALT levels, and hepatic TG levels. (K) Hepatic Acta2, Col1a1, and Timp1 gene expression; n=6 mice/group. (L) Hepatic α-SMA, collagen- I, and TIMP-1 protein expression levels. (M) Hepatic Tnfa , Il6 , and Il1b gene expression levels. (N) Hepatic F4/80 + cell immunohistochemistry. (O) Representative eWAT H&E staining and F4/80 immunohistochemistry image of HFHCD-fed WT mice treated with or without peretinoin. MASH, metabolic dysfunction-associated steatohepatitis; ATG16L1, autophagy-related protein 16-like 1; BMDMs, bone marrow-derived macrophages; STING, stimulator of interferon genes; PAOA, palmitic acid- and oleic acid; CM, conditioned media; HFHCD, high-fat and high-cholesterol diet; <t>MCD,</t> <t>methionine-</t> and choline-deficient diet; NAS, NAFLD activity score; ALT, alanine aminotransferase; TG, hepatic triglyceride; eWAT, epididymal white adipose tissue. The data are expressed as the mean±SD. * P <0.05, ** P <0.01 (unpaired t test or ANOVA).
Methionine Choline Deficient (Mcd) Diet, supplied by research diets inc, 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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Pharmacological enhancement of ATG16L1 expression prevents MASH development. The protein expression levels of STING signaling components in activated WT BMDMs treated with CM from PAOA-stimulated hepatocytes with or without the ATG16L1 enhancer peretinoin following DMXAA stimulation. (B) The protein levels of p-JNK, JNK, c-Jun, and c-Fos in activated WT BMDMs treated with CM. (C) The proinflammatory protein expression levels, (D) proinflammatory gene expression levels, and (E) Ifnb1 and (F) Tgfb1 mRNA expression in activated WT BMDMs treated with CM. (G) Schematic representation of HFHCD-fed or MCD-fed WT mice supplemented with dietary peretinoin. (H) Hepatic ATG16L1 protein expression levels. (I) Hepatic H&E staining, oil red O staining, Sirius red staining, and α-SMA immunohistochemistry. (J) NAS, serum ALT levels, and hepatic TG levels. (K) Hepatic Acta2, Col1a1, and Timp1 gene expression; n=6 mice/group. (L) Hepatic α-SMA, collagen- I, and TIMP-1 protein expression levels. (M) Hepatic Tnfa , Il6 , and Il1b gene expression levels. (N) Hepatic F4/80 + cell immunohistochemistry. (O) Representative eWAT H&E staining and F4/80 immunohistochemistry image of HFHCD-fed WT mice treated with or without peretinoin. MASH, metabolic dysfunction-associated steatohepatitis; ATG16L1, autophagy-related protein 16-like 1; BMDMs, bone marrow-derived macrophages; STING, stimulator of interferon genes; PAOA, palmitic acid- and oleic acid; CM, conditioned media; HFHCD, high-fat and high-cholesterol diet; MCD, methionine- and choline-deficient diet; NAS, NAFLD activity score; ALT, alanine aminotransferase; TG, hepatic triglyceride; eWAT, epididymal white adipose tissue. The data are expressed as the mean±SD. * P <0.05, ** P <0.01 (unpaired t test or ANOVA).

Journal: Clinical and Molecular Hepatology

Article Title: Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy

doi: 10.3350/cmh.2024.0107

Figure Lengend Snippet: Pharmacological enhancement of ATG16L1 expression prevents MASH development. The protein expression levels of STING signaling components in activated WT BMDMs treated with CM from PAOA-stimulated hepatocytes with or without the ATG16L1 enhancer peretinoin following DMXAA stimulation. (B) The protein levels of p-JNK, JNK, c-Jun, and c-Fos in activated WT BMDMs treated with CM. (C) The proinflammatory protein expression levels, (D) proinflammatory gene expression levels, and (E) Ifnb1 and (F) Tgfb1 mRNA expression in activated WT BMDMs treated with CM. (G) Schematic representation of HFHCD-fed or MCD-fed WT mice supplemented with dietary peretinoin. (H) Hepatic ATG16L1 protein expression levels. (I) Hepatic H&E staining, oil red O staining, Sirius red staining, and α-SMA immunohistochemistry. (J) NAS, serum ALT levels, and hepatic TG levels. (K) Hepatic Acta2, Col1a1, and Timp1 gene expression; n=6 mice/group. (L) Hepatic α-SMA, collagen- I, and TIMP-1 protein expression levels. (M) Hepatic Tnfa , Il6 , and Il1b gene expression levels. (N) Hepatic F4/80 + cell immunohistochemistry. (O) Representative eWAT H&E staining and F4/80 immunohistochemistry image of HFHCD-fed WT mice treated with or without peretinoin. MASH, metabolic dysfunction-associated steatohepatitis; ATG16L1, autophagy-related protein 16-like 1; BMDMs, bone marrow-derived macrophages; STING, stimulator of interferon genes; PAOA, palmitic acid- and oleic acid; CM, conditioned media; HFHCD, high-fat and high-cholesterol diet; MCD, methionine- and choline-deficient diet; NAS, NAFLD activity score; ALT, alanine aminotransferase; TG, hepatic triglyceride; eWAT, epididymal white adipose tissue. The data are expressed as the mean±SD. * P <0.05, ** P <0.01 (unpaired t test or ANOVA).

Article Snippet: Mice were randomly assigned to receive a normal chow diet (NCD), a high-fat and high-cholesterol diet (HFHCD) (Research Diets, Inc., New Brunswick, CA, USA) for 16 weeks (n=6–8 per group), or a methionine- and choline-deficient (MCD) diet (Research Diets, Inc.) for 6 weeks (n=6–8 per group).

Techniques: Expressing, Staining, Immunohistochemistry, Derivative Assay, Activity Assay