Fig 1: Sodium butyrate alleviates LPS-induced liver injury and inflammation. (A) H&E staining, immunohistochemical staining for MPO and TUNEL staining of liver tissue in C57BL/6 mice treated with SB, SB + LPS, LPS, and the vehicle group (magnification, ×200). (B) Histology score of hemorrhage, MPO index, and apoptosis index was calculated from TUNEL staining in C57BL/6 mice treated with SB, SB + LPS, LPS, and the vehicle group. (C) Serum levels of ALT and AST were detected using ELISA kits in female C57BL/6 mice treated with normal saline, SB, LPS, and SB + LPS. (D) RT-PCR was used to determine relative mRNA levels of TNF-a, IL-6, and IL-1ß in liver tissues.*P < 0.05 vs vehicle group; #P < 0.05 vs LPS group. Values are expressed as mean ± SD (n = 10 in each group). MPO, myeloperoxidase; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; SB, sodium butyrate; LPS, lipopolysaccharide; ALT, alanine aminotransferase; AST, aspartate transaminase.
Fig 2: GPR43 deficiency interrupted the protection of sodium butyrate on LPS-induced liver injury and inflammation. (A) H&E staining, immunohistochemical staining for MPO, and TUNEL staining of liver tissue in female GPR43 KO mice and WT littermates treated with SB, SB + LPS, LPS, and normal saline (magnification, ×200). (B) Histology score of hemorrhage, MPO index, and the apoptosis index was calculated from TUNEL staining in female GPR43 KO mice and WT littermates treated with SB, SB + LPS, LPS, and normal saline. (C) Serum levels of ALT and AST were detected using ELISA kits. (D) RT-PCR was used to determine relative mRNA levels of TNF-a, IL-6, and IL-1ß in liver tissues. *P < 0.05 vs vehicle group in the same type of mice; #P < 0.05 vs LPS group in the same type of mice; ? P < 0.05 vs SB + LPS group in GPR43 WT mice. Values are expressed as mean ± SD (n = 6 per group). MPO, myeloperoxidase; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling; SB, sodium butyrate; LPS, lipopolysaccharide; ALT, alanine aminotransferase; AST, aspartate transaminase; RT-PCR, real-time polymerase chain reaction.
Fig 3: Bifidobacterium animalis ssp. lactis MG741 (MG741) ameliorates high-fat-diet-induced metabolic disorder parameters. (A) Fasting blood glucose; (B) insulin; (C) HOMA-IR; (D) serum ALT; (E) serum AST; (F) serum leptin; (G) serum total cholesterol; (H) serum HDL-cholesterol; (I) serum LDL-cholesterol; (J) liver weight; and (K) liver triglycerides. Data are presented as the mean ± standard error of the mean (n = 9). The different letters (a–c) indicate significant differences (p < 0.05) determined by one-way ANOVA with Tukey’s post hoc tests.
Fig 4: Changes in the weight of mice over 12 weeks after administration of Western diet with or without oral/IP metformin (A). Western diet resulted in a significant elevation of the serum levels of AST (B), ALT (C), total cholesterol (D), and serum triglycerides (E). Both oral and IP metformin were able to ameliorate these changes. The oral route had better outcomes for AST and ALT levels. For inflammatory markers, the Western diet resulted in a significant elevation of the serum levels of IL-1ß (F), IL-6 (G), IL-17 (H), and TNF-a (I). Except for TNF-a, oral and IP metformin were equally effective in reducing the elevated serum levels of these cytokines in comparison to the Western diet only (n = 10 for each group; * significant (p < 0.05) from the control group; # significant from the Western diet only group, ? significant from the Western diet + IP metformin group; IP: intraperitoneal; Met: metformin; ND: normal diet; TG: triglycerides; WD: Western diet).
Supplier Page from CUSABIO Technology LLC for Mouse Alanine Aminotransferase(ALT/GPT)ELISA Kit