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MedChemExpress lim animals
<t>Quercetin</t> inhibits the PI3K signaling pathway and affects glycolysis. A.PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2 and LDHA expression detected by Western blot in NC, <t>LIM,</t> DMSO, Que-L, Que-M, Que-H group in 4w and 6w. Samples derived from the same experiment and that blots were processed in parallel. B–U. Bar graphs of Western blot analysis for PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2, and LDHA in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. (∗∗∗P < 0.001). V. PIK3Ca, AKT1, FOXO3a immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. W. HK2, PFKL, and LDHA immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w.
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Biotium viability assay kit
<t>Quercetin</t> inhibits the PI3K signaling pathway and affects glycolysis. A.PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2 and LDHA expression detected by Western blot in NC, <t>LIM,</t> DMSO, Que-L, Que-M, Que-H group in 4w and 6w. Samples derived from the same experiment and that blots were processed in parallel. B–U. Bar graphs of Western blot analysis for PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2, and LDHA in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. (∗∗∗P < 0.001). V. PIK3Ca, AKT1, FOXO3a immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. W. HK2, PFKL, and LDHA immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w.
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Jackson Laboratory transgenic notch reporter animals
Notch signaling regulates integrin-β4 levels and delamination. (A-D) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (A) and E16 WT littermate versus Rbpj cKO epidermis (C), with single channel images of integrin-β4 on the right, and associated quantification of fluorescence intensity (B,D); n =3 except for WT control in Rbpj cohort ( n =2). (E-G) Images of Notch reporter (NR) <t>transgenic</t> (E) and LUGGIGE NR-transduced epidermis (F), and associated quantification (G). NR shown in green; RFP marks cells transduced with reporter. (H) Quantification of nuclear YAP in Itgb4 4124 epidermis. (I,K) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (I) and E16 WT littermate versus Rbpj cKO epidermis (K); asterisks indicate dual-positive cells. (J,L) Quantification of dual-positive cells in WT versus mutant. Each dot represents a biological replicate in G,H,J,L, or FOV in B,D, where shapes designate litters. Basement membrane is indicated with cyan dashed line. Scale bars: 25 μm (A,C,E,F,I,K); 10 µm (F, insets). ns, not significant; * P <0.05; **** P <0.0001 ( t -test).
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Data Sciences International animal pulmonary function system
Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small <t>animal</t> dynamic imaging <t>system.</t> Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) <t>Pulmonary</t> oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.
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Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small <t>animal</t> dynamic imaging <t>system.</t> Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) <t>Pulmonary</t> oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.
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Sangon Biotech column animal genomic dna purification kit
Galectin-1 promotes <t>GCPM</t> through <t>the</t> <t>TGF-β/Smad</t> signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.
Column Animal Genomic Dna Purification Kit, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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World Precision Instruments feedback controlled d c temperature controller
Galectin-1 promotes <t>GCPM</t> through <t>the</t> <t>TGF-β/Smad</t> signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.
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FUJIFILM VisualSonics Inc small animal ultrasound imaging system
APOE KO improving mechanical properties of regenerated aortas. <t>Ultrasound</t> detection of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (a) and Day 90 (b). (c) M mode images of ultrasound of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. Arrow heads indicate movement of vascular walls. Quantification of RI (d), PI (e) and compliance (f) of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. ∗∗ indicates p < 0.01, N.S. indicates non-significant, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). Tensile tests and elastic modulus of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (g) and Day 90 (h). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five independent tests of five different samples from five different animals were conducted (n = 5).
Small Animal Ultrasound Imaging System, supplied by FUJIFILM VisualSonics Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Mallinckrodt small animal magnetic resonance facility
APOE KO improving mechanical properties of regenerated aortas. <t>Ultrasound</t> detection of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (a) and Day 90 (b). (c) M mode images of ultrasound of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. Arrow heads indicate movement of vascular walls. Quantification of RI (d), PI (e) and compliance (f) of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. ∗∗ indicates p < 0.01, N.S. indicates non-significant, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). Tensile tests and elastic modulus of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (g) and Day 90 (h). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five independent tests of five different samples from five different animals were conducted (n = 5).
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Image Search Results


Quercetin inhibits the PI3K signaling pathway and affects glycolysis. A.PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2 and LDHA expression detected by Western blot in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. Samples derived from the same experiment and that blots were processed in parallel. B–U. Bar graphs of Western blot analysis for PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2, and LDHA in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. (∗∗∗P < 0.001). V. PIK3Ca, AKT1, FOXO3a immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. W. HK2, PFKL, and LDHA immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w.

Journal: Redox Biology

Article Title: Quercetin improves retinal glycolysis to slow myopia progression through orchestrating the AKT/FOXO/HK2 axis

doi: 10.1016/j.redox.2026.104139

Figure Lengend Snippet: Quercetin inhibits the PI3K signaling pathway and affects glycolysis. A.PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2 and LDHA expression detected by Western blot in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. Samples derived from the same experiment and that blots were processed in parallel. B–U. Bar graphs of Western blot analysis for PIK3Ca、p- PIK3Ca 、AKT1、p-AKT1, FOXO3a, p -FOXO3a, HK2, PFKL, PKM2, and LDHA in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. (∗∗∗P < 0.001). V. PIK3Ca, AKT1, FOXO3a immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w. W. HK2, PFKL, and LDHA immunofluorescence staining in NC, LIM, DMSO, Que-L, Que-M, Que-H group in 4w and 6w.

Article Snippet: To evaluate the effect of quercetin on myopia progression, we used quercetin with a purity of ≥98.06% (HY-18085, MCE, China) to treat LIM animals.

Techniques: Expressing, Western Blot, Derivative Assay, Immunofluorescence, Staining

Effect of quercetin on retinal metabolism in myopia。 A. Mitochondrial membrane potential was detected in NC, LIM, DMSO, Que-L, Que-M, and Que-H groups at 6 weeks. B. Bar graphs of Mitochondrial membrane potential analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). C. ROS were detected in NC, LIM, DMSO, Que-L, Que-M, and Que-H groups at 6 weeks. D. Bar graphs of ROS analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). E. Bar graphs of LA analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). F. Mitochondrial respiratory function in the retina after 6 weeks of myopia induction. G. Bar graphs of basal mitochondrial respiration analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05). H. Bar graphs of maximal mitochondrial respiration analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05). I. Glycolytic function in the retina after 6 weeks of myopia induction. J. Bar graphs of glycolytic capacity analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01). K. Bar graphs of glycolytic reserve analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗P < 0.01, ∗P < 0.05). L. KEGG analysis of metabolites. M. Metabolite expression levels in NC, LIM, and quercetin intervention groups were analyzed by metabonomics. Blue line: glycolytic pathway; Green line: pentose phosphate pathway; Purple line: hexose branch.

Journal: Redox Biology

Article Title: Quercetin improves retinal glycolysis to slow myopia progression through orchestrating the AKT/FOXO/HK2 axis

doi: 10.1016/j.redox.2026.104139

Figure Lengend Snippet: Effect of quercetin on retinal metabolism in myopia。 A. Mitochondrial membrane potential was detected in NC, LIM, DMSO, Que-L, Que-M, and Que-H groups at 6 weeks. B. Bar graphs of Mitochondrial membrane potential analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). C. ROS were detected in NC, LIM, DMSO, Que-L, Que-M, and Que-H groups at 6 weeks. D. Bar graphs of ROS analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). E. Bar graphs of LA analysis in NC, LIM, DMSO, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗P < 0.05). F. Mitochondrial respiratory function in the retina after 6 weeks of myopia induction. G. Bar graphs of basal mitochondrial respiration analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05). H. Bar graphs of maximal mitochondrial respiration analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05). I. Glycolytic function in the retina after 6 weeks of myopia induction. J. Bar graphs of glycolytic capacity analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗∗P < 0.001, ∗∗P < 0.01). K. Bar graphs of glycolytic reserve analysis in NC, LIM, Que-L, Que-M, Que-H group (∗∗P < 0.01, ∗P < 0.05). L. KEGG analysis of metabolites. M. Metabolite expression levels in NC, LIM, and quercetin intervention groups were analyzed by metabonomics. Blue line: glycolytic pathway; Green line: pentose phosphate pathway; Purple line: hexose branch.

Article Snippet: To evaluate the effect of quercetin on myopia progression, we used quercetin with a purity of ≥98.06% (HY-18085, MCE, China) to treat LIM animals.

Techniques: Membrane, Expressing

Effects of quercetin on retinal neurons in myopia. A. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups. B. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups. C. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, DMSO, Que-L, Que-M, Que-H groups. D. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗P < 0.001, ∗P < 0.05). E. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001. ∗∗P < 0.01). F. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001. ∗∗P < 0.01). G. The synapses of the NC, LIM, Que-H, sh-Fos-5ul, and LIM + Fos groups were detected by TEM. The red arrows indicate synapses. H. The mitochondria of the NC, LIM, Que-H, sh-Fos-5ul, and LIM + Fos groups were detected by TEM. The green arrows indicate mitochondria. I: The TEM was used to measure the synaptic lengths of the NC, LIM, Que-H, sh-Fos-5ul and LIM + Fos groups. J. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). K. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001, ∗∗P < 0.01, ∗P < 0.05). L. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). M. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). N. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001, ∗P < 0.05). O. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001).

Journal: Redox Biology

Article Title: Quercetin improves retinal glycolysis to slow myopia progression through orchestrating the AKT/FOXO/HK2 axis

doi: 10.1016/j.redox.2026.104139

Figure Lengend Snippet: Effects of quercetin on retinal neurons in myopia. A. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups. B. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups. C. 5-Min data of Ca2+ (pmol·cm −2 ·s −1 ) in the retina recorded by non-invasive micro-test technology after myopic induction for 6 weeks in NC, LIM, DMSO, Que-L, Que-M, Que-H groups. D. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗P < 0.001, ∗P < 0.05). E. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001. ∗∗P < 0.01). F. Analysis of the retinal Ca 2+ (pmol·cm −2 ·s −1 ) based on NMT for 6 weeks in NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001. ∗∗P < 0.01). G. The synapses of the NC, LIM, Que-H, sh-Fos-5ul, and LIM + Fos groups were detected by TEM. The red arrows indicate synapses. H. The mitochondria of the NC, LIM, Que-H, sh-Fos-5ul, and LIM + Fos groups were detected by TEM. The green arrows indicate mitochondria. I: The TEM was used to measure the synaptic lengths of the NC, LIM, Que-H, sh-Fos-5ul and LIM + Fos groups. J. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). K. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001, ∗∗P < 0.01, ∗P < 0.05). L. The mean values of axial length in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). M. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, LIM + Fos, LIM + Empty, NC + Fos, NC + Empty groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001). N. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, empty, sh-Fos-1ul, sh-Fos-3ul, sh-Fos-5ul groups (∗∗∗∗P < 0.0001, ∗P < 0.05). O. The mean values of refraction in the right eyes of the guinea pigs after myopia induction for 0, 4, and 6 weeks between the NC, LIM, DMSO, Que-L, Que-M, Que-H groups (∗∗∗∗P < 0.0001, ∗∗∗P < 0.001).

Article Snippet: To evaluate the effect of quercetin on myopia progression, we used quercetin with a purity of ≥98.06% (HY-18085, MCE, China) to treat LIM animals.

Techniques:

Notch signaling regulates integrin-β4 levels and delamination. (A-D) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (A) and E16 WT littermate versus Rbpj cKO epidermis (C), with single channel images of integrin-β4 on the right, and associated quantification of fluorescence intensity (B,D); n =3 except for WT control in Rbpj cohort ( n =2). (E-G) Images of Notch reporter (NR) transgenic (E) and LUGGIGE NR-transduced epidermis (F), and associated quantification (G). NR shown in green; RFP marks cells transduced with reporter. (H) Quantification of nuclear YAP in Itgb4 4124 epidermis. (I,K) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (I) and E16 WT littermate versus Rbpj cKO epidermis (K); asterisks indicate dual-positive cells. (J,L) Quantification of dual-positive cells in WT versus mutant. Each dot represents a biological replicate in G,H,J,L, or FOV in B,D, where shapes designate litters. Basement membrane is indicated with cyan dashed line. Scale bars: 25 μm (A,C,E,F,I,K); 10 µm (F, insets). ns, not significant; * P <0.05; **** P <0.0001 ( t -test).

Journal: Development (Cambridge, England)

Article Title: Hemidesmosomes and Notch signaling regulate epidermal differentiation via delamination

doi: 10.1242/dev.205210

Figure Lengend Snippet: Notch signaling regulates integrin-β4 levels and delamination. (A-D) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (A) and E16 WT littermate versus Rbpj cKO epidermis (C), with single channel images of integrin-β4 on the right, and associated quantification of fluorescence intensity (B,D); n =3 except for WT control in Rbpj cohort ( n =2). (E-G) Images of Notch reporter (NR) transgenic (E) and LUGGIGE NR-transduced epidermis (F), and associated quantification (G). NR shown in green; RFP marks cells transduced with reporter. (H) Quantification of nuclear YAP in Itgb4 4124 epidermis. (I,K) Confocal images of E17 Cre-negative control versus Rosa NICD epidermis (I) and E16 WT littermate versus Rbpj cKO epidermis (K); asterisks indicate dual-positive cells. (J,L) Quantification of dual-positive cells in WT versus mutant. Each dot represents a biological replicate in G,H,J,L, or FOV in B,D, where shapes designate litters. Basement membrane is indicated with cyan dashed line. Scale bars: 25 μm (A,C,E,F,I,K); 10 µm (F, insets). ns, not significant; * P <0.05; **** P <0.0001 ( t -test).

Article Snippet: Transgenic Notch reporter animals were obtained from The Jackson Laboratory [ Tg(Cp-EGFP)25Gaia/J, stock #005854].

Techniques: Negative Control, Fluorescence, Control, Transgenic Assay, Transduction, Mutagenesis, Membrane

Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Article Snippet: Pulmonary function was assessed using a small animal pulmonary function system (Data Sciences International, Buxco system, DSI, USA).

Techniques: Ex Vivo, Fluorescence, Imaging, Labeling, In Vivo, Marker, Staining, Activity Assay, Immunofluorescence

Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6).

Techniques: Animal Model, Staining, Immunofluorescence, Fluorescence

Inhibition of TGF-β1 attenuates peritoneal MMT and suppresses GCPM (A) Schematic representation of the carcinomatosis models. (B) Representative gross images of peritoneal carcinomatosis and corresponding H&E staining (×400 magnification). (C) PCI across experimental groups ( n = 6). (D–F) Representative immunofluorescence images showing expression of TGF-β1, p -Smad2/3, and E-cadherin/vimentin in peritoneal tissues from model mice (×400 magnification). (G and H) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). (I and J) Mean fluorescence density of vimentin and E-cadherin ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01.

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Inhibition of TGF-β1 attenuates peritoneal MMT and suppresses GCPM (A) Schematic representation of the carcinomatosis models. (B) Representative gross images of peritoneal carcinomatosis and corresponding H&E staining (×400 magnification). (C) PCI across experimental groups ( n = 6). (D–F) Representative immunofluorescence images showing expression of TGF-β1, p -Smad2/3, and E-cadherin/vimentin in peritoneal tissues from model mice (×400 magnification). (G and H) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). (I and J) Mean fluorescence density of vimentin and E-cadherin ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01.

Article Snippet: Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6).

Techniques: Inhibition, Staining, Immunofluorescence, Expressing, Fluorescence

APOE KO improving mechanical properties of regenerated aortas. Ultrasound detection of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (a) and Day 90 (b). (c) M mode images of ultrasound of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. Arrow heads indicate movement of vascular walls. Quantification of RI (d), PI (e) and compliance (f) of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. ∗∗ indicates p < 0.01, N.S. indicates non-significant, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). Tensile tests and elastic modulus of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (g) and Day 90 (h). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five independent tests of five different samples from five different animals were conducted (n = 5).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: APOE KO improving mechanical properties of regenerated aortas. Ultrasound detection of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (a) and Day 90 (b). (c) M mode images of ultrasound of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. Arrow heads indicate movement of vascular walls. Quantification of RI (d), PI (e) and compliance (f) of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 and Day 90. ∗∗ indicates p < 0.01, N.S. indicates non-significant, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). Tensile tests and elastic modulus of native and regenerated aortas in WT and Apoe −/− rats, respectively, on Day 30 (g) and Day 90 (h). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five independent tests of five different samples from five different animals were conducted (n = 5).

Article Snippet: A small animal ultrasound imaging system (VisualSonics, Vevo 3100, FUJIFILM) was used to evaluate graft performance in WT and Apoe −/− rats after implantation in vivo for 30 or 90 days, respectively.

Techniques:

Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Article Snippet: A small animal ultrasound imaging system (VisualSonics, Vevo 3100, FUJIFILM) was used to evaluate graft performance in WT and Apoe −/− rats after implantation in vivo for 30 or 90 days, respectively.

Techniques: In Vivo, shRNA, Injection, Staining, Immunofluorescence, Enzyme-linked Immunosorbent Assay