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Evaluation of COA-SA/CLT-siSnail micelles in treatment of UUO. (A) Representative H&E and Masson staining images of kidney tissue sections from patients with CKD. Scale bars, 50 μm. (B) Representative α -SMA and E-cadherin immunofluorescence staining images from kidney tissue sections of patients with CKD. Scale bars, 100 μm. (C) Flow diagram of treatment of different preparations against UUO-induced renal fibrosis. (D) Cr and BUN levels on Day 14 after treatment. (E) Contralateral renal index (left) and ligation side renal index (right) of UUO mice after treatment. (F) Renal tubular injury score of UUO mice following treatment. (G) The percentage of collagen area in renal tissue section by Masson staining. (H) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (I) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in sham and UUO mice on Day 14. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . UUO; # P < 0.05; ## P < 0.01; ### P < 0.001; #### P < 0.0001 vs . sham. ns, not significant.
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Evaluation of COA-SA/CLT-siSnail micelles in treatment of UUO. (A) Representative H&E and Masson staining images of kidney tissue sections from patients with CKD. Scale bars, 50 μm. (B) Representative α -SMA and E-cadherin immunofluorescence staining images from kidney tissue sections of patients with CKD. Scale bars, 100 μm. (C) Flow diagram of treatment of different preparations against UUO-induced renal fibrosis. (D) Cr and BUN levels on Day 14 after treatment. (E) Contralateral renal index (left) and ligation side renal index (right) of UUO mice after treatment. (F) Renal tubular injury score of UUO mice following treatment. (G) The percentage of collagen area in renal tissue section by Masson staining. (H) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (I) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in sham and UUO mice on Day 14. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . UUO; # P < 0.05; ## P < 0.01; ### P < 0.001; #### P < 0.0001 vs . sham. ns, not significant.
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Evaluation of COA-SA/CLT-siSnail micelles in treatment of UUO. (A) Representative H&E and Masson staining images of kidney tissue sections from patients with CKD. Scale bars, 50 μm. (B) Representative α -SMA and E-cadherin immunofluorescence staining images from kidney tissue sections of patients with CKD. Scale bars, 100 μm. (C) Flow diagram of treatment of different preparations against UUO-induced renal fibrosis. (D) Cr and BUN levels on Day 14 after treatment. (E) Contralateral renal index (left) and ligation side renal index (right) of UUO mice after treatment. (F) Renal tubular injury score of UUO mice following treatment. (G) The percentage of collagen area in renal tissue section by Masson staining. (H) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (I) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in sham and UUO mice on Day 14. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . UUO; # P < 0.05; ## P < 0.01; ### P < 0.001; #### P < 0.0001 vs . sham. ns, not significant.
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PSP inhibits hepatic collagen production in liver fibrosis-induced rats. Detection of the liver fibrosis markers (A) HA, (B) LN, (C) PIIINP and (D) Col IV in serum samples was performed by ELISA. (E) Expression levels of Col I and <t>Col</t> <t>III</t> in the liver were detected by immunohistochemistry; scale bar, 20 µm. Semi-quantification of (F) Col I and (G) Col III. ELISA was used to detect the levels of (H) Col I and (I) Col III in liver tissue. (J) Levels of Hyp in the liver tissues were detected by ELISA. Data are presented as the mean ± standard deviation, n=6. ### P<0.001 vs. the control group; *P<0.05, **P<0.01 and ***P<0.001 vs. the model group. BJRG, Biejia ruangan; Col, collagen; H, high; HA, hyaluronic acid; Hyp, hydroxyproline; L, low; LN, laminin; PIIINP, procollagen III N-terminal peptide; PSP, Polygonatum sibiricum polysaccharide.
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Image Search Results


Evaluation of COA-SA/CLT-siSnail micelles in treatment of UUO. (A) Representative H&E and Masson staining images of kidney tissue sections from patients with CKD. Scale bars, 50 μm. (B) Representative α -SMA and E-cadherin immunofluorescence staining images from kidney tissue sections of patients with CKD. Scale bars, 100 μm. (C) Flow diagram of treatment of different preparations against UUO-induced renal fibrosis. (D) Cr and BUN levels on Day 14 after treatment. (E) Contralateral renal index (left) and ligation side renal index (right) of UUO mice after treatment. (F) Renal tubular injury score of UUO mice following treatment. (G) The percentage of collagen area in renal tissue section by Masson staining. (H) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (I) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in sham and UUO mice on Day 14. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . UUO; # P < 0.05; ## P < 0.01; ### P < 0.001; #### P < 0.0001 vs . sham. ns, not significant.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Targeting renal tubular epithelial cells via a dual functionalized oligosaccharide self-assembly in the management of acute and chronic kidney diseases

doi: 10.1016/j.apsb.2025.09.017

Figure Lengend Snippet: Evaluation of COA-SA/CLT-siSnail micelles in treatment of UUO. (A) Representative H&E and Masson staining images of kidney tissue sections from patients with CKD. Scale bars, 50 μm. (B) Representative α -SMA and E-cadherin immunofluorescence staining images from kidney tissue sections of patients with CKD. Scale bars, 100 μm. (C) Flow diagram of treatment of different preparations against UUO-induced renal fibrosis. (D) Cr and BUN levels on Day 14 after treatment. (E) Contralateral renal index (left) and ligation side renal index (right) of UUO mice after treatment. (F) Renal tubular injury score of UUO mice following treatment. (G) The percentage of collagen area in renal tissue section by Masson staining. (H) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (I) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in sham and UUO mice on Day 14. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . UUO; # P < 0.05; ## P < 0.01; ### P < 0.001; #### P < 0.0001 vs . sham. ns, not significant.

Article Snippet: Anti-collagen I (COL I) antibody (GB11022-3), anti- α -SMA antibody (GB13044), anti-Vimentin antibody (GB11192), and anti-Fibronectin (FN) antibody ( GB114057 ) were purchased from Servicebio (Wuhan, China).

Techniques: Staining, Immunofluorescence, Ligation, Immunohistochemical staining, Control

Evaluation of COA-SA/CLT-siSnail micelles in treatment of FA-CKD. (A) Flow diagram of the treatment of free CLT solution, COA-SA/CLT micelles, free siSnail solution, COA-SA/siSnail micelles, COA-SA/CLT-siSnail micelles, and COA-SA/CLT-siNC micelles against folate-induced renal fibrosis. (B) Renal index of FA-CKD mice after treatment. (C) Cr and BUN levels on Day 30 after treatment. (D) Renal tubular injury score of FA-CKD mice following treatment. (E) The percentage of collagen area in renal tissue section by Masson staining. (F) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (G) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in FA-CKD mice on Day 30 after treatment. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . FA-CKD; # P < 0.05; ## P < 0.01 vs . vehicle. ns, not significant.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Targeting renal tubular epithelial cells via a dual functionalized oligosaccharide self-assembly in the management of acute and chronic kidney diseases

doi: 10.1016/j.apsb.2025.09.017

Figure Lengend Snippet: Evaluation of COA-SA/CLT-siSnail micelles in treatment of FA-CKD. (A) Flow diagram of the treatment of free CLT solution, COA-SA/CLT micelles, free siSnail solution, COA-SA/siSnail micelles, COA-SA/CLT-siSnail micelles, and COA-SA/CLT-siNC micelles against folate-induced renal fibrosis. (B) Renal index of FA-CKD mice after treatment. (C) Cr and BUN levels on Day 30 after treatment. (D) Renal tubular injury score of FA-CKD mice following treatment. (E) The percentage of collagen area in renal tissue section by Masson staining. (F) Average optical density analysis for COL I, COL IV, FN, VIM, α -SMA, E-CAD, and SNAIL immunohistochemical staining. (G) Real-time qPCR analysis of renal mRNA levels of Acta2 , Col1a1 , Col4a1 , Cadh1 , Fn-1 , Vim , and Snai1 in FA-CKD mice on Day 30 after treatment. GAPDH mRNA as internal control. Data represent mean ± SD ( n = 5). ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001; ∗∗∗∗ P < 0.0001 vs . FA-CKD; # P < 0.05; ## P < 0.01 vs . vehicle. ns, not significant.

Article Snippet: Anti-collagen I (COL I) antibody (GB11022-3), anti- α -SMA antibody (GB13044), anti-Vimentin antibody (GB11192), and anti-Fibronectin (FN) antibody ( GB114057 ) were purchased from Servicebio (Wuhan, China).

Techniques: Staining, Immunohistochemical staining, Control

PSP inhibits hepatic collagen production in liver fibrosis-induced rats. Detection of the liver fibrosis markers (A) HA, (B) LN, (C) PIIINP and (D) Col IV in serum samples was performed by ELISA. (E) Expression levels of Col I and Col III in the liver were detected by immunohistochemistry; scale bar, 20 µm. Semi-quantification of (F) Col I and (G) Col III. ELISA was used to detect the levels of (H) Col I and (I) Col III in liver tissue. (J) Levels of Hyp in the liver tissues were detected by ELISA. Data are presented as the mean ± standard deviation, n=6. ### P<0.001 vs. the control group; *P<0.05, **P<0.01 and ***P<0.001 vs. the model group. BJRG, Biejia ruangan; Col, collagen; H, high; HA, hyaluronic acid; Hyp, hydroxyproline; L, low; LN, laminin; PIIINP, procollagen III N-terminal peptide; PSP, Polygonatum sibiricum polysaccharide.

Journal: Molecular Medicine Reports

Article Title: Polygonatum sibiricum polysaccharide alleviates liver fibrosis through the TGF-β/Smad signaling pathway and reduces collagen

doi: 10.3892/mmr.2025.13599

Figure Lengend Snippet: PSP inhibits hepatic collagen production in liver fibrosis-induced rats. Detection of the liver fibrosis markers (A) HA, (B) LN, (C) PIIINP and (D) Col IV in serum samples was performed by ELISA. (E) Expression levels of Col I and Col III in the liver were detected by immunohistochemistry; scale bar, 20 µm. Semi-quantification of (F) Col I and (G) Col III. ELISA was used to detect the levels of (H) Col I and (I) Col III in liver tissue. (J) Levels of Hyp in the liver tissues were detected by ELISA. Data are presented as the mean ± standard deviation, n=6. ### P<0.001 vs. the control group; *P<0.05, **P<0.01 and ***P<0.001 vs. the model group. BJRG, Biejia ruangan; Col, collagen; H, high; HA, hyaluronic acid; Hyp, hydroxyproline; L, low; LN, laminin; PIIINP, procollagen III N-terminal peptide; PSP, Polygonatum sibiricum polysaccharide.

Article Snippet: Goat serum (cat. no. c-0005), MMP2 (cat. no. bs4605R), MMP9 (cat. no. bsm55544m), Col III (cat no. bs-0549R) and Col I (cat no. bs-7158R) antibodies were obtained from Bioss.

Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Immunohistochemistry, Standard Deviation, Control