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Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining <t>of</t> <t>α-SMA</t> in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard <t>deviation;</t> <t>α-SMA:</t> alpha-smooth muscle actin; Veh: vehicle.
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Fig. 4. Effects of HF on pulmonary vascular proliferation in HAPH rats. <t>(A)</t> <t>α-SMA</t> expressions of representative pulmonary arterioles were stained by IHC in each group of rats (magnification × 100/400 and scale bar = 100 μm). (B–D) Changes of proliferative indicators PCNA, CDK6, Cyclin D1 expressions in lung tissue of rats were detected by WB in each group. (E) Change of antiproliferative indicator p21 expression in lung tissue of rats was detected by WB in each group. Original blots are presented in Supplementary information. The data are expressed as the mean ± SD, n = 3 per group. $P < 0.05, $$P < 0.01, *P < 0.05, **P < 0.01 vs. the Nor group; #P < 0.05 vs. the Hyp group.
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Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining of α-SMA in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard deviation; α-SMA: alpha-smooth muscle actin; Veh: vehicle.

Journal: Cardiology Plus

Article Title: Cepharanthine aggravated atherosclerosis and liver injury in Apoe −/− and Ldlr −/− mice

doi: 10.1097/cp9.0000000000000109

Figure Lengend Snippet: Figure 3. Cep induced liver damage. A, Serum levels of AST and ALT in Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 9 for each group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice; B, Gross images of liver from Apoe−/− and Ldlr−/− mice treated with or without Cep. n = 6 for the Veh group and n = 7 for the Cep group in Apoe−/− mice; n = 8 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 1 cm; C, Liver weight and liver weight index in Apoe−/− and Ldlr−/− mice treated with or without Cep; D, H&E staining of livers from Apoe−/− and Ldlr−/− mice treated with or without Cep. Both internal and peripheral liver sections were captured. n = 9 for the Veh group and n = 8 for the Cep group in Apoe−/− mice; n = 7 for the Veh group and n = 6 for the Cep group in Ldlr−/− mice. Scale bar: 20 μm; E, Sirius red staining of liver sections from Apoe−/− and Ldlr−/− mice treated with or without Cep. Internal and peripheral liver sections were captured. Scale bar: 50 μm; F, Immunofluorescence staining of COL1A1 in liver sections from Apoe−/− and Ldlr−/− mice. Scale bar: 50 μm. n = 5 for each group; G, Immunofluorescence staining of α-SMA in liver sections from Apoe−/− and Ldlr−/− mice liver. Scale bar: 100 μm. n = 5 for each group. All data are presented as the means ± SD. Data for ALT in Apoe−/− mice, and AST and ALT in Ldlr−/− mice were analyzed using the Kolmogorov- Smirnov test. Data for AST in Apoe−/− mice were analyzed using an unpaired Student t test. For C, liver weight in Apoe−/− mice was analyzed using the Kolmogorov-Smirnov test; liver weight index in Apoe−/− mice, and liver weight and liver weight index in Ldlr−/− mice were analyzed using an unpaired Student t test. ALT: alanine aminotransferase; AST: aspartate aminotransferase; Cep: cepharanthine; COL1A1: collagen type I alpha 1; DAPI: 4’-6-diamidino-2- phenylindole; H&E: hematoxylin and eosin; SD: standard deviation; α-SMA: alpha-smooth muscle actin; Veh: vehicle.

Article Snippet: Primary antibodies include rabbit anti-mouse α-SMA antibody (14395-1-AP; Proteintech, Rosemont, Illinois, USA) and collagen type I monoclonal antibody (67288-1- Ig; Proteintech), both diluted at 1:500.

Techniques: Staining, Immunofluorescence, Standard Deviation

Journal: Cell Reports Medicine

Article Title: Spatially resolved transcriptomics reveal the determinants of primary resistance to immunotherapy in NSCLC with mature tertiary lymphoid structures

doi: 10.1016/j.xcrm.2025.101934

Figure Lengend Snippet:

Article Snippet: Anti-α-SMA (D4K9N) Rabbit Monoclonal Primary Antibody , CST , 19245.

Techniques: Software, Clinical Proteomics, Imaging

Fig. 4. Effects of HF on pulmonary vascular proliferation in HAPH rats. (A) α-SMA expressions of representative pulmonary arterioles were stained by IHC in each group of rats (magnification × 100/400 and scale bar = 100 μm). (B–D) Changes of proliferative indicators PCNA, CDK6, Cyclin D1 expressions in lung tissue of rats were detected by WB in each group. (E) Change of antiproliferative indicator p21 expression in lung tissue of rats was detected by WB in each group. Original blots are presented in Supplementary information. The data are expressed as the mean ± SD, n = 3 per group. $P < 0.05, $$P < 0.01, *P < 0.05, **P < 0.01 vs. the Nor group; #P < 0.05 vs. the Hyp group.

Journal: Scientific reports

Article Title: Halofuginone prevents inflammation and proliferation of high-altitude pulmonary hypertension by inhibiting the TGF-β1/Smad signaling pathway.

doi: 10.1038/s41598-025-88258-z

Figure Lengend Snippet: Fig. 4. Effects of HF on pulmonary vascular proliferation in HAPH rats. (A) α-SMA expressions of representative pulmonary arterioles were stained by IHC in each group of rats (magnification × 100/400 and scale bar = 100 μm). (B–D) Changes of proliferative indicators PCNA, CDK6, Cyclin D1 expressions in lung tissue of rats were detected by WB in each group. (E) Change of antiproliferative indicator p21 expression in lung tissue of rats was detected by WB in each group. Original blots are presented in Supplementary information. The data are expressed as the mean ± SD, n = 3 per group. $P < 0.05, $$P < 0.01, *P < 0.05, **P < 0.01 vs. the Nor group; #P < 0.05 vs. the Hyp group.

Article Snippet: All immunohistochemical (IHC) reagents, RIPA buffer, PMSF, BCA protein assay kit, primary antibodies against α-SMA (Cat. No. 19245), PCNA (Cat. No. 13110), CDK6 (Cat. No. 3136), Cyclin D1 (Cat. No. 55506), Smad2/3 (Cat. No. 8685), p-Smad2/3 (Cat. No. 8828), β-actin (Cat. No. 4970), and Anti-rabbit (Cat. No. 7074)/mouse (Cat. No. 7076) IgG, HRP-linked antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Staining, Expressing