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lps  (Cusabio)
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Cusabio lps
Fig. 5. Effects of HFDF on placental inflammation associ- ated with impaired gut barrier and placental bacterial components <t>(LPS)</t> translocation in GDM model. Schematic of the maternal diet regimen and breeding is shown in Fig. 2A. At E18.5, serum and intestinal samples were obtained after execution of mice. (A) Representative colon images and colon length (n = 10 mice per group). (B, E, and F) Representative H&E staining images of colon sections, histological score, and goblet cell (yellow dashed lines) number per colonic crypt (n = 6 mice per group). Scale bar, 200 μm. (C and G) Representative Alcian blue–periodic acid Schiff (AB-PAS) staining images of colon sections and quantification of mucus secretion (white arrows) (n = 6 mice per group). Scale bar, 200 μm. (D and H) Representative Picrosirius red of colon sections and quantifi- cation (n = 6 mice per group). (I to K) <t>Serum</t> <t>DAO,</t> LPS, and FITC-dextran flux levels (n = 6 mice per group). FITC-dextran flux was analyzed in another independent experiment. (L to O) Immunoblots and quantification of barrier-forming tight junction markers and TLR4/NF-κB inflammatory pathway in colon (n = 6 mice per group). (P) 4 Expression levels of cyto- kines and inflammatory-related factors in placenta (n = 6 mice per group). (Q) Placental LPS level in women (non-GDMs, n = 42; GDMs, n = 21). (R) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in women. (S) Placental LPS level in mice (n = 6 placentae from 6 litters per group). (T) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in mice. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (A to P and S) or unpaired Student’s t test with Welch’s correction (Q) and represented means ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, relative to chow group or non-GDM. #P < 0.05, ##P < 0.01, and ###P < 0.001, relative to GDM group.
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Fig. 5. Effects of HFDF on placental inflammation associ- ated with impaired gut barrier and placental bacterial components <t>(LPS)</t> translocation in GDM model. Schematic of the maternal diet regimen and breeding is shown in Fig. 2A. At E18.5, serum and intestinal samples were obtained after execution of mice. (A) Representative colon images and colon length (n = 10 mice per group). (B, E, and F) Representative H&E staining images of colon sections, histological score, and goblet cell (yellow dashed lines) number per colonic crypt (n = 6 mice per group). Scale bar, 200 μm. (C and G) Representative Alcian blue–periodic acid Schiff (AB-PAS) staining images of colon sections and quantification of mucus secretion (white arrows) (n = 6 mice per group). Scale bar, 200 μm. (D and H) Representative Picrosirius red of colon sections and quantifi- cation (n = 6 mice per group). (I to K) <t>Serum</t> <t>DAO,</t> LPS, and FITC-dextran flux levels (n = 6 mice per group). FITC-dextran flux was analyzed in another independent experiment. (L to O) Immunoblots and quantification of barrier-forming tight junction markers and TLR4/NF-κB inflammatory pathway in colon (n = 6 mice per group). (P) 4 Expression levels of cyto- kines and inflammatory-related factors in placenta (n = 6 mice per group). (Q) Placental LPS level in women (non-GDMs, n = 42; GDMs, n = 21). (R) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in women. (S) Placental LPS level in mice (n = 6 placentae from 6 litters per group). (T) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in mice. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (A to P and S) or unpaired Student’s t test with Welch’s correction (Q) and represented means ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, relative to chow group or non-GDM. #P < 0.05, ##P < 0.01, and ###P < 0.001, relative to GDM group.
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Fig. 5. Effects of HFDF on placental inflammation associ- ated with impaired gut barrier and placental bacterial components <t>(LPS)</t> translocation in GDM model. Schematic of the maternal diet regimen and breeding is shown in Fig. 2A. At E18.5, serum and intestinal samples were obtained after execution of mice. (A) Representative colon images and colon length (n = 10 mice per group). (B, E, and F) Representative H&E staining images of colon sections, histological score, and goblet cell (yellow dashed lines) number per colonic crypt (n = 6 mice per group). Scale bar, 200 μm. (C and G) Representative Alcian blue–periodic acid Schiff (AB-PAS) staining images of colon sections and quantification of mucus secretion (white arrows) (n = 6 mice per group). Scale bar, 200 μm. (D and H) Representative Picrosirius red of colon sections and quantifi- cation (n = 6 mice per group). (I to K) <t>Serum</t> <t>DAO,</t> LPS, and FITC-dextran flux levels (n = 6 mice per group). FITC-dextran flux was analyzed in another independent experiment. (L to O) Immunoblots and quantification of barrier-forming tight junction markers and TLR4/NF-κB inflammatory pathway in colon (n = 6 mice per group). (P) 4 Expression levels of cyto- kines and inflammatory-related factors in placenta (n = 6 mice per group). (Q) Placental LPS level in women (non-GDMs, n = 42; GDMs, n = 21). (R) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in women. (S) Placental LPS level in mice (n = 6 placentae from 6 litters per group). (T) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in mice. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (A to P and S) or unpaired Student’s t test with Welch’s correction (Q) and represented means ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, relative to chow group or non-GDM. #P < 0.05, ##P < 0.01, and ###P < 0.001, relative to GDM group.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of <t>serum</t> <t>Cys-C</t> concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.
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Image Search Results


Fig. 5. Effects of HFDF on placental inflammation associ- ated with impaired gut barrier and placental bacterial components (LPS) translocation in GDM model. Schematic of the maternal diet regimen and breeding is shown in Fig. 2A. At E18.5, serum and intestinal samples were obtained after execution of mice. (A) Representative colon images and colon length (n = 10 mice per group). (B, E, and F) Representative H&E staining images of colon sections, histological score, and goblet cell (yellow dashed lines) number per colonic crypt (n = 6 mice per group). Scale bar, 200 μm. (C and G) Representative Alcian blue–periodic acid Schiff (AB-PAS) staining images of colon sections and quantification of mucus secretion (white arrows) (n = 6 mice per group). Scale bar, 200 μm. (D and H) Representative Picrosirius red of colon sections and quantifi- cation (n = 6 mice per group). (I to K) Serum DAO, LPS, and FITC-dextran flux levels (n = 6 mice per group). FITC-dextran flux was analyzed in another independent experiment. (L to O) Immunoblots and quantification of barrier-forming tight junction markers and TLR4/NF-κB inflammatory pathway in colon (n = 6 mice per group). (P) 4 Expression levels of cyto- kines and inflammatory-related factors in placenta (n = 6 mice per group). (Q) Placental LPS level in women (non-GDMs, n = 42; GDMs, n = 21). (R) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in women. (S) Placental LPS level in mice (n = 6 placentae from 6 litters per group). (T) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in mice. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (A to P and S) or unpaired Student’s t test with Welch’s correction (Q) and represented means ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, relative to chow group or non-GDM. #P < 0.05, ##P < 0.01, and ###P < 0.001, relative to GDM group.

Journal: Science advances

Article Title: Lachnospiraceae -derived butyrate mediates protection of high fermentable fiber against placental inflammation in gestational diabetes mellitus.

doi: 10.1126/sciadv.adi7337

Figure Lengend Snippet: Fig. 5. Effects of HFDF on placental inflammation associ- ated with impaired gut barrier and placental bacterial components (LPS) translocation in GDM model. Schematic of the maternal diet regimen and breeding is shown in Fig. 2A. At E18.5, serum and intestinal samples were obtained after execution of mice. (A) Representative colon images and colon length (n = 10 mice per group). (B, E, and F) Representative H&E staining images of colon sections, histological score, and goblet cell (yellow dashed lines) number per colonic crypt (n = 6 mice per group). Scale bar, 200 μm. (C and G) Representative Alcian blue–periodic acid Schiff (AB-PAS) staining images of colon sections and quantification of mucus secretion (white arrows) (n = 6 mice per group). Scale bar, 200 μm. (D and H) Representative Picrosirius red of colon sections and quantifi- cation (n = 6 mice per group). (I to K) Serum DAO, LPS, and FITC-dextran flux levels (n = 6 mice per group). FITC-dextran flux was analyzed in another independent experiment. (L to O) Immunoblots and quantification of barrier-forming tight junction markers and TLR4/NF-κB inflammatory pathway in colon (n = 6 mice per group). (P) 4 Expression levels of cyto- kines and inflammatory-related factors in placenta (n = 6 mice per group). (Q) Placental LPS level in women (non-GDMs, n = 42; GDMs, n = 21). (R) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in women. (S) Placental LPS level in mice (n = 6 placentae from 6 litters per group). (T) Two-tailed Pearson’s correlation coefficient analysis of placental LPS levels and placental TNF-α in mice. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (A to P and S) or unpaired Student’s t test with Welch’s correction (Q) and represented means ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001, relative to chow group or non-GDM. #P < 0.05, ##P < 0.01, and ###P < 0.001, relative to GDM group.

Article Snippet: The levels of TNF-α (MM-0132 M1 and MM-0122H1, MEIMIAN, China), insulin (MM-0579 M1, MEIMIAN), HbA1c (MM-1517H1 and MM-0159 M2, MEIMIAN, China), LPS (CSB-E13066m, Cusabio, China; MM-1309H1, MM-0634 M1, and MEIMIAN, China), and DAO (CSB-E10090m, Cusabio, China) were measured with commercial kits as instructed by the respective manufacturers.

Techniques: Translocation Assay, Staining, Western Blot, Expressing, Two Tailed Test

Fig. 8. Effects of Lachnospiraceae and SCFAs on HFD-induced placental inflammation and GDM development. (A) Schematic of medium control [brain-heart in- fusion (BHI)], transfer experiments with bacteria (Lachnospiraceae), Lachnospiraceae + β-acid (an inhibitor of bacterial SCFA production), acetate, or butyrate. At E18.5, serum, intestinal, and placental samples were obtained after execution of mice (n = 6 mice per group). (B and C) Serum and placental LPS level (n = 6 mice per group). (D and E) Serum and placental TNF-α level (n = 6 mice per group). (F) GTT and AUC (n = 6 mice per group). (G) ITT and AUC (n = 6 mice per group). (H and K) Immuno- histochemistry and quantification of CCL2 (one of the key factors in macrophage recruitment) in placenta (n = 6 placentae from 6 litters per group). Scale bar, 200 μm. (I, L, and M) Localization of macrophage (F4/80+; red), M1 macrophage (iNOS+/F4/80+; green/red; yellow arrow), and M2 macrophage (CD206+ F4/80+; pink/red; it was not quantified because it was almost nonexistent) in placenta by immunofluorescence (n = 6 placentae from 6 litters per group). Scale bar, 50 μm. (J and N) Localization of Treg cell (Foxp3+/CD4+; yellow arrow) in placenta by immunofluorescence (n = 6 placentae from 6 litters per group). Scale bar, 50 μm. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (B to E, AUC, and K to N) or two-way ANOVA followed by post hoc Bonferroni tests (GTT and ITT) and represented means ± SEM. & and $P < 0.05, && and $$P < 0.01, and &&& and $$$P < 0.001, with & versus BHI-Recip and $ versus Lachnospiraceae-Recip.

Journal: Science advances

Article Title: Lachnospiraceae -derived butyrate mediates protection of high fermentable fiber against placental inflammation in gestational diabetes mellitus.

doi: 10.1126/sciadv.adi7337

Figure Lengend Snippet: Fig. 8. Effects of Lachnospiraceae and SCFAs on HFD-induced placental inflammation and GDM development. (A) Schematic of medium control [brain-heart in- fusion (BHI)], transfer experiments with bacteria (Lachnospiraceae), Lachnospiraceae + β-acid (an inhibitor of bacterial SCFA production), acetate, or butyrate. At E18.5, serum, intestinal, and placental samples were obtained after execution of mice (n = 6 mice per group). (B and C) Serum and placental LPS level (n = 6 mice per group). (D and E) Serum and placental TNF-α level (n = 6 mice per group). (F) GTT and AUC (n = 6 mice per group). (G) ITT and AUC (n = 6 mice per group). (H and K) Immuno- histochemistry and quantification of CCL2 (one of the key factors in macrophage recruitment) in placenta (n = 6 placentae from 6 litters per group). Scale bar, 200 μm. (I, L, and M) Localization of macrophage (F4/80+; red), M1 macrophage (iNOS+/F4/80+; green/red; yellow arrow), and M2 macrophage (CD206+ F4/80+; pink/red; it was not quantified because it was almost nonexistent) in placenta by immunofluorescence (n = 6 placentae from 6 litters per group). Scale bar, 50 μm. (J and N) Localization of Treg cell (Foxp3+/CD4+; yellow arrow) in placenta by immunofluorescence (n = 6 placentae from 6 litters per group). Scale bar, 50 μm. Data were analyzed by one-way ANOVA followed by post hoc Tukey’s tests (B to E, AUC, and K to N) or two-way ANOVA followed by post hoc Bonferroni tests (GTT and ITT) and represented means ± SEM. & and $P < 0.05, && and $$P < 0.01, and &&& and $$$P < 0.001, with & versus BHI-Recip and $ versus Lachnospiraceae-Recip.

Article Snippet: The levels of TNF-α (MM-0132 M1 and MM-0122H1, MEIMIAN, China), insulin (MM-0579 M1, MEIMIAN), HbA1c (MM-1517H1 and MM-0159 M2, MEIMIAN, China), LPS (CSB-E13066m, Cusabio, China; MM-1309H1, MM-0634 M1, and MEIMIAN, China), and DAO (CSB-E10090m, Cusabio, China) were measured with commercial kits as instructed by the respective manufacturers.

Techniques: Control, Bacteria, Immunohistochemistry, Immunofluorescence

Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of serum Cys-C concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.

Journal: Pharmaceutical Biology

Article Title: Qigui didang decoction alleviates renal injury in a diabetic kidney disease model with metabolic memory features: association with ferroptosis and the SIRT1/Nrf2 pathway

doi: 10.1080/13880209.2026.2648168

Figure Lengend Snippet: Experimental procedure, general condition, and biochemical indices of rats in each group. A: Flowchart of SD rat modeling and grouping; B: Bar charts of week 20 blood glucose levels across groups; C: Line chart showing dynamic changes in body weight of rats in each group from weeks 0 to 20; D: Line charts of blood glucose dynamics from weeks 8–20; E: Weight difference of each group; F: Bar chart of 24-UTP levels in rats from each group; G: Bar chart of serum BUN concentration in each group; H: Bar chart of serum scr concentration in each group; I: Bar chart of serum β2-MG concentration in each group; J: Bar chart of serum Cys-C concentration in each group; K: Bar graph depicting serum T-CHO concentrations in each group of rats; L: Bar graph depicting serum TG concentrations in each group of rats; M: Bar graph depicting renal tissue TG concentrations in each group of rats; N: Bar graph depicting renal tissue HDL-C concentrations in each group of rats; O: Bar graph depicting renal tissue T-CHO concentrations in each group of rats; P: Bar graph depicting renal tissue LDL-C concentrations in each group of rats; Compared to group C, ** p < 0.01, * p < 0.05, ns p > 0.05; Compared to group M, △△ p < 0.01, △ p < 0.05, ▽ p > 0.05; Compared to the Met group, ▲▲ p < 0.01, ▲ p < 0.05, ▼ p > 0.05.

Article Snippet: Reagents and Kits: Metformin (Solarbio, Cat# D9351); STZ (Solarbio, Cat# S8050); Hematoxylin (Servicebio, Cat# G1004); Eosin (Solarbio, Cat# G1100); Masson’s trichrome staining kit (Servicebio, Cat# G1006); Prussian blue staining kit (Solarbio, Cat# G1422); Modified Oil Red O staining kit (Solarbio, Cat# G1263); Assay kits for reduced glutathione (GSH, Nanjing Jiancheng Bioengineering Institute, Cat# A006-1-1), total cholesterol (TCH/T-CHO, Cat# A111-1-1), triglycerides (TG, Cat# A110-1-1), total superoxide dismutase (T-SOD, Cat# A001-3-2), malondialdehyde (MDA, Cat# A003-1-2), blood urea nitrogen (BUN, Cat# C013-2-1), creatinine (Cr, Cat# C011-2-1), high-density lipoprotein cholesterol (HDL-C, Cat# A112-1-1), low-density lipoprotein cholesterol (LDL-C, Cat# A113-1-1), urinary protein quantification (Cat# F006-1-1), and cystatin C (Cys-C, Cat# C035-2-1); Ferrous ion detection kit (Solarbio, Cat# BC5415); Rat cystatin C (Cys-C) ELISA kit and rat β2-microglobulin (β2-MG) ELISA kit (Jiangsu Meimian Industrial Co., Cat# MM-0438R1 and MM-21246R1, respectively); TUNEL apoptosis detection kit (Servicebio, Cat# G1502); DAPI (Beyotime, Cat# C1006); Dihydroethidium (MCE, Cat# PD-MY003); BCA protein assay kit (Boster Biological, Cat# AR0146); Primary antibodies: Nrf2 (Proteintech, Cat# 80593-1-RR), HO-1 (Cat# 10701-1-AP), GPX4 (Cat# 67763-1-Ig), GAPDH (Cat# 60004-1-Ig); ECL chemiluminescence kit (Wuhan Sanying Biotechnology, Cat# PK10003); Secondary antibodies: HRP-conjugated (Proteintech, Cat# SA00001-1), fluorescein-labeled goat anti-rabbit IgG (Cat# SA00001-2), Urethane (SCR, Cat# 20210521).

Techniques: Concentration Assay