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: PLoS ONE

Article Title: Ontogeny of Hepatic Energy Metabolism Genes in Mice as Revealed by RNA-Sequencing

doi: 10.1371/journal.pone.0104560

Figure Lengend Snippet: A) One-way hierarchical cluster map of lipid metabolism genes that changed significantly in at least one age compared to Day 60. mRNA expression of genes that were statistically different from those in mice 60 days of age (control) have the percent indicated within the heatmap square (control = 100%). B) Examples of FPKM (fragments per kilobase of exon per million reads mapped) values of individual genes of lipid metabolism throughout development. C) Western blot analysis of Scd1 protein expression in liver of pre-weaning and post-weaning mice, α-tubulin was used as a loading control. For gene function information see .

Article Snippet: Membranes were then probed with antibodies specific for Scd1 (1∶1000 dilution; 2438S; Cell Signaling Technology, Inc., Danvers, MA) or α-tubulin (1∶5000 dilution; CP06; EMD-Millipore Corp, Billerica, MA).

Techniques: Expressing, Control, Western Blot

Journal: PLoS ONE

Article Title: A proteomics approach for the identification of cullin-9 (CUL9) related signaling pathways in induced pluripotent stem cell models

doi: 10.1371/journal.pone.0248000

Figure Lengend Snippet: CUL9 KO express normal levels of key fatty acid metabolism enzymes SCD1 ( A ) and DHCR24 ( B ) n-3; mean +/- SEM; Analysis done using student’s t-test, α = 0.05. CUL9 KO hPSCs have the same oxygen consumption rate (OCR) ( C ), ATP production ( D ), spare respiratory capacity ( E ), and levels of proton leak ( F ) as parental and isogenic WT hPSCs. CUL9 KO hNPCs also display no abnormalities ( G-J ). n = 3 independent experiments done in triplicate, error bars are +/- SEM. (OCR) was measured using the Seahorse Biosciences Mito Stress Test on an XFe96 analyzer. ATP production was calculated from the corresponding OCR traces in panels A and C for each condition. Spare respiratory capacity is the difference between maximal respiration or basal respiration. Oligomycin inhibits ATP synthase interrupting the electron transport chain ultimately disrupting mitochondrial respiration and ATP production. FCCP is an uncoupler, uncoupling ATP production from the electron transport chain. Rotenone (complex I inhibitor) and antimycin A (complex III inhibitor) completely inhibit mitochondrial respiration, only permitting nonmitochondrial respiration to persist.

Article Snippet: We used antibodies against OCT4 (Cell Signaling Technology, Cat. 75463S), NANOG (Cell Signaling Technology, Cat. 4903S), SOX2 (Cell Signaling Technology, Cat. 5049S), Cleaved Caspase-3 (Cell Signaling Technology, Cat. 9661S), CUL9 (Bethyl Laboratories, Cat. A300-98A), CUL7 (Bethyl Laboratories, Cat. A300-223A), ANAPC7 (Bethyl Laboratories, Cat. A302-551), FZR1 (Abcam, Cat. ab3242), and Cyclin-A2 (Cell Signaling Technology, Cat. 4656T), PAX6 (Cell Signaling Technology Cat. 60433), Nestin (STEMCELL Technologies, Cat. 60091), TUBB3 (Cell Signaling Technology, Cat. 4466S), MAP2 (Thermo Fisher Scientific, Cat. 131500), beta-Actin (Sigma, Cat. A1978), alpha-Tubulin (Sigma, Cat. T9026), and GAPDH (Cell Signaling Technology, Cat. 5147S), SOX3 (Thermo Fisher, Cat. PA5-35983), TM7SF2 (Thermo Scientific, Cat. 12033-1-AP), CUX1 (Abcam, Cat. ab54583), and SCD1 (Bethyl, Laboratories, Cat. A305-259A-T).

Techniques: