Journal: Gut Microbes

Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

doi: 10.1080/19490976.2026.2701349

Figure Lengend Snippet: PSM upregulates hepatic SCD1 by enriching L. johnsonii . (a) Relative gene expression of hepatic SCD1 ( n =6). (b) Hepatic protein level of SCD1 was assessed by Western blotting and the densitometric quantification ( n =3). (c) Schematic diagram of the mouse experiment. (d) Relative expression of hepatic SCD1 and its upstream regulatory genes ( n =6). (e) Protein level of hepatic SCD1 in the CTRL, PSM alone and ABX+PSM groups, along with densitometric quantification ( n =3). (f) Relative abundance of altered microbiota by PSM alone at the genus level ( n =6). (g) Relative abundance of three Lactobacillus species in stool samples quantified by QPCR ( n =5). (h) Differential abundance of the fecal microbiota at the species level ( n =6). (i) Relative abundance of L. johnsonii was increased in the PSM alone group ( n =6). (j) Relative abundance of L. johnsonii in each group ( n =6). (k) Correlation analysis of the relative abundance of L. johnsonii and hepatic SCD1 protein expression. (l) Growth curves of L. johnsonii cultured with different concentrations of PSM at the indicated time points ( n =3). (m) Bacterial colony counts of L. johnsonii . *, # p < 0.05, *, ## p < 0.01, *, ### p < 0.001.

Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

Techniques: Gene Expression, Western Blot, Expressing, Cell Culture

Journal: Gut Microbes

Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

doi: 10.1080/19490976.2026.2701349

Figure Lengend Snippet: L. johnsonii activates hepatic LXRα–SCD1 signaling to ameliorate liver injury and colitis. (a) Schematic diagram of the mouse experiment. (b) Relative expression of LXRα downstream target genes ( n =6). (c) Levels of LXRα–SCD1 signaling pathway-related proteins in mice liver ( n =3). (d) Hepatic immunohistochemistry staining showed increased protein expression (LXRα, SREBP1, FASN and SCD1) by culture supernatant of L. johnsonii (Ljsup) ( n =3). (e) Relative abundance of liver LPC species altered by Ljsup ( n =5–6). (f) Serum LPS, TC and TG concentrations ( n =6). (g) Correlation analysis of differential LPC and LPE species with the serum TC, TG concentrations and hepatic SCD1 protein expression. (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) Colon length, spleen and cecum index on day 8 ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Ljsup supplementation reduced the relative expression of colonic inflammatory cytokines ( n =6). (m) Ljsup supplementation increased the relative expression of colonic ZO-1 ( n =6). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

Techniques: Expressing, Immunohistochemistry, Staining, Activity Assay

Journal: Gut Microbes

Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

doi: 10.1080/19490976.2026.2701349

Figure Lengend Snippet: SR9238 abolishes the liver protection and anti-colitis effects of L. johnsonii . (a) Relative mRNA levels of SREBF1, FASN and SCD1 in HepG2 cells pretreated with insulin (10 µg/ml) for 7 d, followed by 2 µM, 10 µM, and 20 µM SR9238 treatment ( n =3). (b) Schematic diagram of the mouse experiment. (c) Relative expression levels of hepatic SREBF1, FASN and SCD1 in mice ( n =6). (d) Representative images of mice colon, liver and spleen. (e) Masson's trichrome staining showed increased collagen in liver sections (scale bar, 100 µm) ( n =3). (f) Serum TG and TC concentrations ( n =6). (g) Oil Red O staining showed incereased lipid droplet accumulation (scale bar, 100 µm) ( n =3). (h, i) Body weight changes and disease activity index (DAI) changes during the experiment ( n =6). (j) Colon length, spleen and cecum index ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) SR9238 reduced the relative expression of claudin and occludin in colon tissue ( n =5). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

Techniques: Expressing, Staining, Activity Assay

Journal: Gut Microbes

Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

doi: 10.1080/19490976.2026.2701349

Figure Lengend Snippet: CORT aggravates colitis with liver injury through the LXRα‒SCD1 axis. (a) Oil Red O staining of AML12 cells treated with 2 µM, 10 µM, and 50 µM CORT. (b) Schematic diagram of the mouse experiment. (c) Protein levels of hepatic CD36, LXRα, FASN, and SCD1 in mice. (d) Representative immunohistochemical staining revealed the decreased protein expression (LXRα, FASN, SCD1, and CD36) in mice ( n =3). (e) Representative images of mice colon, liver and spleen. (f) Representative H&E, Masson's trichrome and Oil Red staining of liver sections (scale bar, 100 µm) ( n =3). (g) Serum TG and TC concentrations ( n =6). (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) CORT reduced colon length ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Schematic diagram of the mouse experiment. (m, n) Relative mRNA levels of LXRα target genes. (o) Levels of LXRα signaling pathway-related proteins in mouse liver. (p) Serum TG and TC concentrations ( n =6). (q) Disease activity index (DAI) changes during the experiment ( n =6). (r) Colon length on day 12. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, not significant ( p > 0.05).

Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

Techniques: Staining, Immunohistochemical staining, Expressing, Activity Assay

Journal: Foods

Article Title: Chemical Composition Analysis of Highland Barley ( Hordeum vulgare L.) with Different Modification Methods and Lipid Metabolism Mechanism Analysis of Highland Barley with Microwave Fluidization Modification

doi: 10.3390/foods15081396

Figure Lengend Snippet: Protein expression levels ( A , H ) including ( B ) PPARγ, ( C ) Fabp4, ( D ) CD36, ( E ) SREBP-1c, ( F ) ADIPOQ, ( G ) SCD-1, ( I ) TLR4, ( J ) IKKβ, and ( K ) p-P65 in liver tissues among NCD, HFCD, and HFCD + HB-1. Data were expressed as mean ± SD ( n = 3) based on Dunnett’s test. ** indicated p < 0.01, *** indicated p < 0.001, **** indicated p < 0.0001.

Article Snippet: The specific antibody concentrations used in this study were as follows: anti-rabbit antibodies against Peroxisome proliferator-activated receptor γ (PPARγ) (1:1000, 58 kDa, Affinity, 16643-1-AP), FABP4 (1:1000, 15 kDa, Affinity, DF6035), CD36 (1:1000, 88 kDa, Affinity, DF13262), SREBP-1c (1:1000, 122 kDa, Affinity, AF6283), ADIPOQ (1:1000, 26 kDa, Affinity, DF7000), SCD-1 (1:1000, 41 kDa, Bioss, bs-3787R), p-P65 (1:1000, 65 kDa, Affinity, AF2006, Serine Ser536), TLR4 (1:1000, 100 kDa, Affinity, AF7017), IKKβ (1:1000, 87 kDa, Affinity, AF6010), and GAPDH (1:1000, 37 kDa, Xianzhi Biotech, AB-P-R 001).

Techniques: Expressing

Journal: Stem Cells Translational Medicine

Article Title: METTL1-deficient mesenchymal stem cells protect against metabolic-associated fatty liver disease by increasing NAMPT secretion

doi: 10.1093/stcltm/szag016

Figure Lengend Snippet: METTL1-deficient MSCs inhibit lipid synthesis in hepatocytes. (A) Representative images of Nile Red staining in hepatocytes co-cultured with MSC shGFP and MSC shMETTL1 following treatment with FFA (Scale bar = 20 μm). (B) Measurement of TG content in hepatocytes in the indicated groups. (C, D) Western blot analysis of lipid metabolism-related gene expression (FASN, SREBP1, SCD1) in the indicated groups. (E, F) qPCR analysis of lipid synthesis gene expression ( Fasn, Scd1, Srebp1, Fads1 and Acaca ) in AML12 and HepG2 cells co-cultured with MSC shGFP and MSC shMETTL1 . For all statistical graphs, data are presented as mean ± S.E.M, with statistical significance is indicated in the figure.

Article Snippet: Primary antibodies specific for the following proteins were obtained from Cell Signaling Technology: ACC-1 (#3676), SCD1 (#2794), FASN (#3180), p-AKT (#4060), and AKT (#9272).

Techniques: Staining, Cell Culture, Western Blot, Gene Expression

Journal: Stem Cells Translational Medicine

Article Title: METTL1-deficient mesenchymal stem cells protect against metabolic-associated fatty liver disease by increasing NAMPT secretion

doi: 10.1093/stcltm/szag016

Figure Lengend Snippet: Transplantation of METTL1-deficient MSCs alleviates metabolic disorders associated with MASLD. (A) Schematic diagram of the animal experiment. (B) Evaluation of liver weight and the liver-to-body weight ratio in the indicated mice. (C) Assessment of fasting blood glucose levels in the indicated mice. (D) Analysis of GTT and ITT for the indicated groups. (E) Measurement of serum ALT and AST levels following 7 weeks of cell transplantation. (F) Representative images of HE and Oil Red O staining for analysis of mouse liver tissue (Scale bar = 100 μm). (G) Determination of TG and TC levels in the liver tissue of the specified mice. (H) qPCR analysis of lipid synthesis-related genes, including Fasn, Scd1, Srebp1, Fads1 , and Acaca in the specified groups. (I) Western blot analysis of lipid metabolism-related proteins in the specified groups. For all statistical graphs, individual data points represent individual mice, and data are presented as mean ± S.E.M. Statistical significance is indicated as shown in the figure.

Article Snippet: Primary antibodies specific for the following proteins were obtained from Cell Signaling Technology: ACC-1 (#3676), SCD1 (#2794), FASN (#3180), p-AKT (#4060), and AKT (#9272).

Techniques: Transplantation Assay, Staining, Western Blot