assay kits  (Elabscience Biotechnology)

Journal: Gastroenterology

Article Title: A Gut-Restricted Liver X Receptor Agonist Ameliorates Liver Injury in Experimental Short Bowel Syndrome

doi: 10.1053/j.gastro.2025.12.015

Figure Lengend Snippet: Aggravated IFALD following the deficiency of intestinal ApoA1 and HDL-C after SBR. ( A–D ) WT male ( filled circles ) or female ( open circles ) mice underwent sham or SBR. Starting 3 weeks later, mice received daily vehicle or WUSTL0717 (30 mg/kg, PO) for 7 weeks, followed by analysis (n = 5–9/group). ( A ) Heatmap of cholesterol efflux–related transcripts in the duodenum and post-anastomosis ileum from male mice (n = 3–4/group). ( B ) qRT-PCR analysis of Apoa1 transcripts in the duodenum, post-anastomosis ileum, and liver (n = 4–9/group). ( C and D ) Portal venous HDL-C ( C ) and ApoA1 ( D ) levels from males (plasma) and females (serum) (n = 5–9/group). ( E and F ) Correlation of portal venous plasma HDL-C and ApoA1 levels with liver collagen area ( , upper ). Each dot represents a matched individual from ( C ) and ( D ). ( G–M ) Apoa1 ΔIEC mice underwent SBR and were euthanized 11 weeks later. Dark dots represent males and light dots represent females (males, n = 7/group; females: n = 6–7/group). ( G and H ) Portal venous serum HDL-C and ApoA1 levels. ( I ) Systemic (inferior vena cava) serum ALT levels. ( J ) Liver Col1a1 transcript levels analyzed by qRT-PCR. ( K ) Sirius Red–stained liver sections ( scale bar , 200 μ m) with quantification from 5 to 6 areas per liver, 1 image per mouse (males, n = 7/group; females: n = 6–7/group). ( L and M ) Correlation of portal venous serum HDL-C and ApoA1 levels with liver collagen area. Each dot represents a matched individual from ( K )–( M ). Statistical evaluations were done using unpaired Student t test ( C , G–K ), 1-way analysis of variance with Tukey’s honestly significant difference ( B , D ), or Pearson correlation ( E , F , L , and M ).

Article Snippet: HDL-cholesterol (HDL-C) levels were measured using the HDL-C assay kit (STA-394; Cell Biolabs), and ApoA1 levels by enzyme-linked immunosorbent assay (3750–1HP; Mabtech).

Techniques: Quantitative RT-PCR, Clinical Proteomics, Staining

Journal: Frontiers in Nutrition

Article Title: Redistribution of branched-chain amino acid intake between active and inactive phases modulates hepatic metabolism in rats

doi: 10.3389/fnut.2026.1754879

Figure Lengend Snippet: Experimental design, growth, intake partitioning, skeletal-muscle S6 signaling, and endpoint plasma markers under phase-shifted BCAA regimens. (A) Simplified study design: rats were maintained on a 12-h light:12-h dark cycle and assigned for 12 weeks to Ctrl (AIN-93G throughout), D + N − (BCAA+20 during the light/inactive phase and BCAA−20 during the dark/active phase), or D − N + (BCAA−20 during the light/inactive phase and BCAA+20 during the dark/active phase), where BCAA+20 and BCAA−20 denote diets containing ~20% higher or lower total BCAA content than Ctrl, respectively; daily energy and nitrogen were intended to be matched while allowing minor day-to-day variation during implementation ( n = 6/group). (B,C) Individual body weight trajectories from week 0 (acclimation) to weeks 1–12 (experimental period) (B) and weekly body weight distributions shown as boxplots (weeks 1–12) with pairwise between-group comparisons annotated above brackets (C) . (D,E) Representative immunoblots of total ribosomal protein S6 and phosphorylated S6 (p-S6, Ser235/236) in skeletal muscle at the end of the study, with total protein staining (TPS; Ponceau S) used for normalization ( n = 4/group; region approximately ~32 kDa displayed) (D) , and densitometric quantification of S6/TPS, p-S6/TPS, and phosphorylation ratio (p-S6/S6 computed as (p-S6/TPS)/(S6/TPS)) with individual animals overlaid (E) . (F) Weekly feed intake partitioned by circadian phase (inactive/light phase: 07:00–19:00; active/dark phase: 19:00–07:00); within each week, upper brackets/ p -values compare whole-day (24 h) total intake between the groups, and lower brackets/ p -values compare inactive vs. active intake within each group (red p-values indicate p < 0.05 as displayed). (G) Endpoint fasting plasma HDL-C, LDL-C, triglycerides (TG), total cholesterol (TC), and malondialdehyde (MDA) across the groups (units as indicated on axes). Group colors follow Ctrl (red), D − N + (green), and D + N − (blue). Boxplots show median and interquartile range (IQR), whiskers extend to 1.5 × IQR, and points indicate individual values (with outliers beyond whiskers where shown). Pairwise statistics were computed using two-sided t-tests with Holm p -value adjustment.

Article Snippet: Specifically, serum lipids were quantified by measuring total cholesterol (TC) using the Total Cholesterol (TC) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K109-M), high-density lipoprotein cholesterol (HDL-C) using the HDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) using the LDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K205-M), malondialdehyde (MDA) using the Malondialdehyde (MDA) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K025-M), and triglycerides (TGs) using the Triglyceride (TG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K261-M).

Techniques: Clinical Proteomics, Western Blot, Staining, Phospho-proteomics

Journal: Frontiers in Pharmacology

Article Title: Effects of Guanxinning tablet on the gut microbiota and bile acid metabolism in mice with hyperlipidemia

doi: 10.3389/fphar.2026.1754769

Figure Lengend Snippet: Effects of GXNT on body weight and lipid metabolism of HFD-fed mice. (A) The animal experimental design; (B) Body weight in the sixth week; (C) Liver index; (D–G) Serum TC, TG, LDL-C, and HDL-C levels. # P < 0.05, ## P < 0.01 compared with the CON group; * P < 0.05, ** P < 0.01 compared with the MOD group.

Article Snippet: The levels of total cholesterol (TC) (E-BC-K109-M), triglycerides (TG) (E-BC-K251-M), high-density lipoprotein cholesterol (HDL-C) (E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) (E-BC-K205-M) and D-Lactic Acid (D-LA) (E-BC-K002-M) in the serum were measured using colorimetric assays using commercial kits (Elabscience, Wuhan, China).

Techniques: