serum hepcidin  (Elabscience Biotechnology)

Journal: Gut Microbes

Article Title: Underlying MASLD-induced gut microbiome dysbiosis and intestinal inflammation are key to poor outcomes in vibriosis infections in a preclinical model

doi: 10.1080/19490976.2026.2652474

Figure Lengend Snippet: Establishment of MASLD pathophysiology in mice by CD-HFD feeding for 20 weeks. (A) Schematic representation of the experimental mouse groups: LEAN [ n = 6; chow diet-fed mice for 20 weeks] and MASLD [ n = 6; CD-HFD fed mice for 20 weeks]. (B) Liver weight (grams), and (C) liver-to-body weight ratio of the LEAN and MASLD mouse groups. Serum levels of (D) ALT (U/L), (E) AST (U/L), (F) hepcidin (ng/mL), and (G) ferritin (μg/mL) in the LEAN and MASLD groups. Formalin-fixed, paraffin-embedded 5 μm liver slices from the LEAN and MASLD groups were used for histopathological analyses. Representative images of (H) hematoxylin and eosin (H&E) staining, picrosirius red (PSR) staining, and immunohistochemistry images depicting α -SMA, and IL-1β immunoreactivity (indicated by black arrowheads) in the liver sections of LEAN and MASLD mouse groups. H&E and immunohistochemistry images were captured at 200× magnification, whereas PSR images were captured at 100× magnification. (I) NAFLD activity score (NAS) and fibrosis score for the LEAN and MASLD groups. Morphometric analyses (calculated as %ROI) of (J) PSR staining, (K) α -SMA, and (L) IL-1β immunoreactivity, where the Y-axis represents % positive immunoreactive area ( n = 3; mean value taken from three separate microscopic fields). The data are presented as mean ± SEM, and statistical significance was tested using unpaired t-test between the two groups, followed by Bonferroni post-hoc corrections (* p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Serum hepcidin (ng/mL) (Catalog No. NBP2-82129, Novus Biologicals, Centennial, CO, USA), ferritin (μg/mL) (Catalog No. KA1941, Novus Biologicals, Centennial, CO, USA), immunoglobulin-A (IgA) (μg/mL) (Catalog No. ab157717, Abcam, Cambridge, MA, USA) and C-reactive protein (CRP) (μg/mL) (Catalog No. MCRP00, Novus Biological, Centennial, CO, USA) were quantified as per the manufacturers’ instructions using commercially available ELISA kits.

Techniques: Formalin-fixed Paraffin-Embedded, Staining, Immunohistochemistry, Activity Assay

Journal: Gut Microbes

Article Title: Underlying MASLD-induced gut microbiome dysbiosis and intestinal inflammation are key to poor outcomes in vibriosis infections in a preclinical model

doi: 10.1080/19490976.2026.2652474

Figure Lengend Snippet: Underlying MASLD conditions in mice caused increased non-cholera vibriosis and affected the hepatic pathophysiology. (A) Schematic representation of the experimental mouse groups: LEAN [ n = 6; chow diet-fed mice for 20 weeks], LEAN + VV [ n = 6; mice fed with chow diet for 20 weeks and received oral VV inoculation for 24 h], MASLD [ n = 6; CD-HFD fed mice for 20 weeks], and MASLD + VV [ n = 6; mice fed with CD-HFD for 20 weeks and received oral VV inoculation for 24 h]. (B) Liver weight (grams), and (C) liver-to-body weight ratio of the LEAN, LEAN + VV, MASLD, and MASLD + VV mouse groups. Serum levels of (D) CRP (μg/mL), (E) ALT (U/L), (F) AST (U/L), (G) hepcidin (ng/mL), and (H) ferritin (μg/mL) in the LEAN, LEAN + VV, MASLD, and MASLD + VV mouse groups. Formalin-fixed, paraffin-embedded 5 μm liver slices from the LEAN, LEAN + VV, MASLD, and MASLD + VV mouse groups were used for histopathological analyses. Representative images of (I) hematoxylin and eosin (H&E) staining and Picrosirius red (PSR) staining of liver sections of LEAN, LEAN + VV, MASLD, and MASLD + VV mouse groups. H&E images were captured at 200× magnification, whereas PSR images were captured at 100× magnification. (J) NAFLD activity score (NAS) and fibrosis score for the LEAN, LEAN + VV, MASLD, and MASLD + VV mouse groups. (K) Morphometric analyses (calculated as %ROI) of PSR staining, where the Y-axis represents % positive immunoreactive area ( n = 3; mean value taken from three separate microscopic fields). Data were represented as mean ± SEM, and statistical significance was tested using one-way ANOVA between all the groups, followed by Bonferroni post-hoc corrections (ns = non-significant, * p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Serum hepcidin (ng/mL) (Catalog No. NBP2-82129, Novus Biologicals, Centennial, CO, USA), ferritin (μg/mL) (Catalog No. KA1941, Novus Biologicals, Centennial, CO, USA), immunoglobulin-A (IgA) (μg/mL) (Catalog No. ab157717, Abcam, Cambridge, MA, USA) and C-reactive protein (CRP) (μg/mL) (Catalog No. MCRP00, Novus Biological, Centennial, CO, USA) were quantified as per the manufacturers’ instructions using commercially available ELISA kits.

Techniques: Formalin-fixed Paraffin-Embedded, Staining, Activity Assay

Journal: Gut Microbes

Article Title: Underlying MASLD-induced gut microbiome dysbiosis and intestinal inflammation are key to poor outcomes in vibriosis infections in a preclinical model

doi: 10.1080/19490976.2026.2652474

Figure Lengend Snippet: FMT in mice with underlying MASLD conditions showed improved pathophysiological outcomes Compared to non-cholera vibriosis infection. (A) Schematic representation of the experimental mouse groups: LEAN + VV [ n = 6; mice fed with chow diet for 20 weeks and received oral VV inoculation for 24 h], LEAN + FMT + VV [ n = 6; chow diet-fed mice, first treated with the ABX cocktail for 15 d followed by FMT for 7 d, and received oral VV inoculation for 24 h], MASLD + VV [ n = 6; mice fed with CD-HFD for 20 weeks and received oral VV inoculation for 24 h], and MASLD + FMT + VV [ n = 6; CD-HFD fed mice, first treated with the ABX cocktail for 15 d followed by FMT for 7 d, and received oral VV inoculation for 24 h]. (B) Liver weight (grams), and (C) liver-to-body weight ratio of the LEAN + VV, LEAN + FMT + VV, MASLD + VV, and MASLD + FMT + VV mouse groups. Serum levels of (D) CRP (μg/mL), (E) ALT (U/L), (F) AST (U/L), (G) Hepcidin (ng/mL), (H) Ferritin (μg/mL) in the LEAN + VV, LEAN + FMT + VV, MASLD + VV, and MASLD + FMT + VV mouse groups. Formalin-fixed, paraffin-embedded 5 μm liver slices were used for histopathological analyses. Representative images of (I) hematoxylin and eosin (H&E) staining and picrosirius red (PSR) staining in the liver sections from the LEAN + VV, LEAN + FMT + VV, MASLD + VV, and MASLD + FMT + VV mouse groups. H&E images were captured at 200× magnification, whereas PSR images were captured at 100× magnification. (J) NAFLD activity score (NAS) and fibrosis score for the LEAN + VV, LEAN + FMT + VV, MASLD + VV, and MASLD + FMT + VV mouse groups. (K) Morphometric analyses (calculated as %ROI) of PSR staining, where the Y-axis represents % positive immunoreactive area ( n = 3; mean value taken from three separate microscopic fields). The data are presented as mean ± SEM, and statistical significance was tested using one-way ANOVA between all the groups, followed by Bonferroni post-hoc corrections (ns = non-significant, * p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Serum hepcidin (ng/mL) (Catalog No. NBP2-82129, Novus Biologicals, Centennial, CO, USA), ferritin (μg/mL) (Catalog No. KA1941, Novus Biologicals, Centennial, CO, USA), immunoglobulin-A (IgA) (μg/mL) (Catalog No. ab157717, Abcam, Cambridge, MA, USA) and C-reactive protein (CRP) (μg/mL) (Catalog No. MCRP00, Novus Biological, Centennial, CO, USA) were quantified as per the manufacturers’ instructions using commercially available ELISA kits.

Techniques: Infection, Formalin-fixed Paraffin-Embedded, Staining, Activity Assay

Journal: Journal of Cachexia, Sarcopenia and Muscle

Article Title: Sex similarities and divergences in systemic and muscle iron metabolism adaptations to extreme physical inactivity in rats

doi: 10.1002/jcsm.13547

Figure Lengend Snippet: Graphical abstract illustrating the impact of extreme physical inactivity and sex on iron metabolism systemic regulation in rats. Unlike in humans, female rats exhibit higher serum, liver, and spleen iron concentrations and serum hepcidin levels than male rats in their basal state. However, there is no difference in iron concentration in the soleus muscle between the sexes in the basal state. In response to 7 days of hindlimb unloading, while both inactive males and females do not show altered plasma iron availability, only males present an increase in spleen and liver iron concentrations and serum hepcidin. However, both sexes exhibit an increase in iron concentration in the soleus muscle. This image was created with BioRender.com .

Article Snippet: Serum hepcidin (S‐1483, BMA Biomedicals, Switzerland) concentrations were measured by enzyme‐linked immunosorbent assay, according to the manufacturer's instructions.

Techniques: Concentration Assay, Clinical Proteomics

Journal: eLife

Article Title: Hormone replacement therapy for postmenopausal atherosclerosis is offset by late age iron deposition

doi: 10.7554/eLife.80494

Figure Lengend Snippet: ( A ) Ferritin (Ft-L), revealed by immunohistochemistry (IHC), and iron content, revealed by DAB-enhanced Prussian blue staining, in plaque paraffin sections of eight postmenopausal patients. Upper panel: the early postmenopausal (EPM) group (P1–P4,<65 years old); lower panel: the late postmenopausal (LPM) group (P5–P8, >65 years old). ( B ) ERα and Ft-L expression in plaques measured by western blotting. The samples are the same as in ( A ) except for the lane switch between lane 6 (P6) and lane 7 (P7) by chance. ( C ) Serum ferritin levels in EPM (blue) and LPM (magenta) patients, detected by ELISA. n = 10/group, ***p<0.001. ( D ) Serum iron measured by using an autochemical analyzer (Beckman Coulter AU5421, CA). n = 10/group, ***p<0.001. ( E ) Serum hepcidin levels detected by ELISA. n = 10/group, ****p<0.0001. ( F ) Serum total cholesterol (left) and total triglyceride (right) levels. n = 10/group, *p<0.05, **p<0.01. Student’s t- test analysis was used for ( C–F ). Figure 1—source data 1. Raw data for .

Article Snippet: eNOS (Abcam, Cambridge, MA), serum hepcidin (Solarbio), and ferritin (US Biological, #F4015-11, Swampscott, MA) were detected by ELISA according to the manufacturer’s protocols.

Techniques: Immunohistochemistry, Staining, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay