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JS-K attenuates autophagic activity in cerebral microvascular endothelial cells after CA/CPR and OGD/R. A Representative immunoblot images and B quantitation of <t>LC3B</t> II and LAMP2 in bEnd.3 cells from Control, OGD/R and OGD/R + JS-K groups. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C The bEnd.3 cells were transfected with RFP-mWasabi-LC3 lentiviral vector in Control, OGD/R, and OGD/R + JS-K groups. Representative images of fluorescent LC3 dots are shown. D Mean number of autophagosomes (dots with both red and green color; i.e., dots with yellow color in merged images) and autolysosomes (dots with only red but not green color; i.e., dots with red color in merged images) per cell. Scale bar = 10 μm. E Representative electron micrographs of bEnd.3 cells in Control, OGD/R and OGD/R + JS-K groups. F The percentage of autophagic vacuoles (white arrows) per cytoplasm area was calculated. Scale bar = 5 μm. G Representative immunoblot images and H quantitation of LC3B II and LAMP2 in cerebral microvessels of mice in Sham, CA/CPR and CA/CPR + JS-K groups at 24 h after ROSC. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments

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1) Product Images from "Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy"

Article Title: Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy

Journal: Cellular and Molecular Neurobiology

doi: 10.1007/s10571-026-01706-w

Figure Legend Snippet: JS-K attenuates autophagic activity in cerebral microvascular endothelial cells after CA/CPR and OGD/R. A Representative immunoblot images and B quantitation of LC3B II and LAMP2 in bEnd.3 cells from Control, OGD/R and OGD/R + JS-K groups. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C The bEnd.3 cells were transfected with RFP-mWasabi-LC3 lentiviral vector in Control, OGD/R, and OGD/R + JS-K groups. Representative images of fluorescent LC3 dots are shown. D Mean number of autophagosomes (dots with both red and green color; i.e., dots with yellow color in merged images) and autolysosomes (dots with only red but not green color; i.e., dots with red color in merged images) per cell. Scale bar = 10 μm. E Representative electron micrographs of bEnd.3 cells in Control, OGD/R and OGD/R + JS-K groups. F The percentage of autophagic vacuoles (white arrows) per cytoplasm area was calculated. Scale bar = 5 μm. G Representative immunoblot images and H quantitation of LC3B II and LAMP2 in cerebral microvessels of mice in Sham, CA/CPR and CA/CPR + JS-K groups at 24 h after ROSC. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments

Techniques Used: Activity Assay, Western Blot, Quantitation Assay, Control, Derivative Assay, Transfection, Plasmid Preparation

Inhibition of HMGB1 nucleocytoplasmic translocation attenuates autophagy and improves endothelial function in bEnd.3 cells. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of fluorescent LC3 dots are shown. F Mean number of autophagosomes and autolysosomes per cell. Scale bar = 10 μm. G The diffusion rates of FITC-dextran (40 kDa). H Representative images of transwell migration assay and I quantitative analysis of migration cells. Scale bar = 100 μm. J Representative images of tube formation assay and K quantitative analysis of total tube length. Scale bar = 100 μm

Figure Legend Snippet: Inhibition of HMGB1 nucleocytoplasmic translocation attenuates autophagy and improves endothelial function in bEnd.3 cells. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of fluorescent LC3 dots are shown. F Mean number of autophagosomes and autolysosomes per cell. Scale bar = 10 μm. G The diffusion rates of FITC-dextran (40 kDa). H Representative images of transwell migration assay and I quantitative analysis of migration cells. Scale bar = 100 μm. J Representative images of tube formation assay and K quantitative analysis of total tube length. Scale bar = 100 μm

Techniques Used: Inhibition, Translocation Assay, Western Blot, Quantitation Assay, Expressing, Control, Derivative Assay, Immunofluorescence, Staining, Diffusion-based Assay, Transwell Migration Assay, Migration, Tube Formation Assay

Inhibition of ATG5 improves endothelial function and BBB function without affecting HMGB1 nucleocytoplasmic translocation. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of tube formation assay and F quantitative analysis of total tube length. Scale bar = 100 μm. G Representative images of transwell migration assay and H quantitative analysis of migration cells. Scale bar = 100 μm. I Representative immunoblot images and J quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in cerebral microvessels of mice from Sham, CA/CPR and CA/CPR + shATG5 groups at 24 h after ROSC. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. K Representative immunofluorescence images of occludin and CD31 co-staining in brain sections at 24 h after ROSC and L Representative immunofluorescence images of ZO-1 and CD31 co-staining in brain sections at 24 h after ROSC and M quantification of occludin and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. N quantification of ZO-1 and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. O BBB permeability evaluated using EB at 24 h after ROSC. P Brain water content of mice at 24 h after ROSC

Figure Legend Snippet: Inhibition of ATG5 improves endothelial function and BBB function without affecting HMGB1 nucleocytoplasmic translocation. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of tube formation assay and F quantitative analysis of total tube length. Scale bar = 100 μm. G Representative images of transwell migration assay and H quantitative analysis of migration cells. Scale bar = 100 μm. I Representative immunoblot images and J quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in cerebral microvessels of mice from Sham, CA/CPR and CA/CPR + shATG5 groups at 24 h after ROSC. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. K Representative immunofluorescence images of occludin and CD31 co-staining in brain sections at 24 h after ROSC and L Representative immunofluorescence images of ZO-1 and CD31 co-staining in brain sections at 24 h after ROSC and M quantification of occludin and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. N quantification of ZO-1 and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. O BBB permeability evaluated using EB at 24 h after ROSC. P Brain water content of mice at 24 h after ROSC

Techniques Used: Inhibition, Translocation Assay, Western Blot, Quantitation Assay, Expressing, Control, Derivative Assay, Immunofluorescence, Staining, Tube Formation Assay, Transwell Migration Assay, Migration, Permeability

Western Blot:

Article Title: Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling
Article Snippet: Caspase 9 , 1:2000 , Cell Signaling Technology , 9508 , WB. .. LC3B-I/II , 1:2000 , Cell Signaling Technology , 2775 , WB. .. pc-Met , 1:2000 , Cell Signaling Technology , 3126 , WB.

other:

Article Title: Increased regional activity of a pro-autophagy pathway in schizophrenia as a contributor to sex differences in the disease pathology
Article Snippet: LC3B-I/II , Cell Signaling Technology , Cat# 43566, RRID: AB_2910544 ).

Membrane:

Article Title: Rapamycin extenuates experimental colitis by modulating the gut microbiota.
Article Snippet: Correspondence Youlian Zhou and Yongjian Zhou, Department of Gastroenterology and Hepatology, School of Medicine, The Second Affiliated Hospital, South China University of Technology, Guangzhou, Guangdong, China.. Email: eyyoulianzhou@scut.edu.cn and eyzhouyongjian@scut.edu.cn Haoming Xu, Department of Gastroenterology and Hepatology, School of Medicine, Guangzhou First People’s Hospital, South China University of Technology, Guangzhou, Guangdong, China.. Email: haomingxu1992@126.com

Article Title: Alisertib exerts KRAS allele‑specific anticancer effects on colorectal cancer cell lines
Article Snippet: Pierce TM bicinchoninic acid (BCA) protein assay kit and radioimmunoprecipitation assay (RIPA) buffer were sourced from Thermo Fisher Scientific, Inc. Western blotting substrate (20X LumiGLO ® Reagent and 20X Peroxide; cat. no. 7003) was purchased from Cell Signaling Technology, Inc. .. Skimmed milk and nitrocellulose membrane were purchased from Bio-Rad Laboratories, Inc. Primary antibodies for cleaved poly ADP-ribose polymerase [PARP, (cat. no. 5625S)], phosphorylated (p-)Akt (Ser473) (cat. no. 4060S), Akt (cat. no. 9272S), p-Erk1/2 (Thr202/Tyr204) (cat. no. 4370S), Erk1/2 (cat. no. 4695S), RAS (cat. no. 3339S) and LC3B-I/II (cat. no. 3868S), and secondary antibodies for rabbit (cat. no. 7074S) and mouse (cat. no. 7076S) were purchased from Cell Signaling Technology, Inc., and β-actin (cat. no. sc-47778) was purchased from Santa Cruz Biotechnology, Inc. All primary antibodies were diluted at 1:1,000 and secondary antibodies were diluted at 1:4,000. .. The well-recognized and commonly used CRC cell lines Caco-2 KRAS WT , Colo-678 KRAS G12D , SK-CO-1 KRAS G12V , HCT116 KRAS G13D , CCCL-18 KRAS A146T and HT29 BRAF V600E were purchased from American Type Culture Collection (ATCC).

Incubation:

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Journal: Cellular and Molecular Neurobiology

Article Title: Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy

doi: 10.1007/s10571-026-01706-w

Figure Lengend Snippet: JS-K attenuates autophagic activity in cerebral microvascular endothelial cells after CA/CPR and OGD/R. A Representative immunoblot images and B quantitation of LC3B II and LAMP2 in bEnd.3 cells from Control, OGD/R and OGD/R + JS-K groups. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C The bEnd.3 cells were transfected with RFP-mWasabi-LC3 lentiviral vector in Control, OGD/R, and OGD/R + JS-K groups. Representative images of fluorescent LC3 dots are shown. D Mean number of autophagosomes (dots with both red and green color; i.e., dots with yellow color in merged images) and autolysosomes (dots with only red but not green color; i.e., dots with red color in merged images) per cell. Scale bar = 10 μm. E Representative electron micrographs of bEnd.3 cells in Control, OGD/R and OGD/R + JS-K groups. F The percentage of autophagic vacuoles (white arrows) per cytoplasm area was calculated. Scale bar = 5 μm. G Representative immunoblot images and H quantitation of LC3B II and LAMP2 in cerebral microvessels of mice in Sham, CA/CPR and CA/CPR + JS-K groups at 24 h after ROSC. β-actin was used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments

Article Snippet: Membranes were blocked with 5% skim milk and incubated with primary antibodies against Occludin (13409-1-AP, RRID:AB_2156308, Proteintech), ZO-1 (21773-1-AP, AB_10733242, Proteintech), LC3B II/I (#3868, RRID:AB_2137707, CST), LAMP2 (bs-2379R, RRID:AB_11048043, Bioss, China), HMGB1 (10829-1-AP, RRID:AB_2232989, Proteintech), ATG5 (10181-2-AP, RRID:AB_2062045, Proteintech) and HRP-conjugated secondary antibodies (1:2 000, bs-0302R, Bioss).

Techniques: Activity Assay, Western Blot, Quantitation Assay, Control, Derivative Assay, Transfection, Plasmid Preparation

Journal: Cellular and Molecular Neurobiology

Article Title: Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy

doi: 10.1007/s10571-026-01706-w

Figure Lengend Snippet: Inhibition of HMGB1 nucleocytoplasmic translocation attenuates autophagy and improves endothelial function in bEnd.3 cells. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + Leptomycin B groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of fluorescent LC3 dots are shown. F Mean number of autophagosomes and autolysosomes per cell. Scale bar = 10 μm. G The diffusion rates of FITC-dextran (40 kDa). H Representative images of transwell migration assay and I quantitative analysis of migration cells. Scale bar = 100 μm. J Representative images of tube formation assay and K quantitative analysis of total tube length. Scale bar = 100 μm

Techniques: Inhibition, Translocation Assay, Western Blot, Quantitation Assay, Expressing, Control, Derivative Assay, Immunofluorescence, Staining, Diffusion-based Assay, Transwell Migration Assay, Migration, Tube Formation Assay

Journal: Cellular and Molecular Neurobiology

Article Title: Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy

doi: 10.1007/s10571-026-01706-w

Figure Lengend Snippet: Inhibition of ATG5 improves endothelial function and BBB function without affecting HMGB1 nucleocytoplasmic translocation. A Representative immunoblot images and B quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. C Representative immunofluorescence images of HMGB1 localization in bEnd.3 cells from Control, OGD/R and OGD/R + ATG5 siRNA groups. HMGB1 (green), nuclei stained with DAPI (blue). Scale bar = 50 μm. D Quantification of nuclear and cytoplasmic HMGB1 signals. Nuclear HMGB1 was defined as HMGB1 signal overlapping with DAPI, and cytoplasmic HMGB1 as non-overlapping HMGB1 signal. E Representative images of tube formation assay and F quantitative analysis of total tube length. Scale bar = 100 μm. G Representative images of transwell migration assay and H quantitative analysis of migration cells. Scale bar = 100 μm. I Representative immunoblot images and J quantitation of nuclear HMGB1, cytoplasmic HMGB1, ATG5, LC3B II, LAMP2, occludin and ZO-1 expression in cerebral microvessels of mice from Sham, CA/CPR and CA/CPR + shATG5 groups at 24 h after ROSC. Histone H3 and β-actin were used as the protein loading control. The images of western blotting data derived from triplicate blots conducted as three independent experiments. K Representative immunofluorescence images of occludin and CD31 co-staining in brain sections at 24 h after ROSC and L Representative immunofluorescence images of ZO-1 and CD31 co-staining in brain sections at 24 h after ROSC and M quantification of occludin and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. N quantification of ZO-1 and CD31 merged area. Scale bars: main panel = 20 μm; zoom-in = 10 μm. O BBB permeability evaluated using EB at 24 h after ROSC. P Brain water content of mice at 24 h after ROSC

Techniques: Inhibition, Translocation Assay, Western Blot, Quantitation Assay, Expressing, Control, Derivative Assay, Immunofluorescence, Staining, Tube Formation Assay, Transwell Migration Assay, Migration, Permeability

MSC therapy reversed the SI-induced increased levels of autophagy markers, increased loss of mitochondrial membrane potential, and increased intracellular ROS contents in R28 cells. (A) A dot plot displays the fluorescence density of J-aggregates (y-axis) against JC-1 monomers (x-axis). (B) Quantitative analysis of the loss of MMP by the red and green fluorescence ratio. (C) DCFH-DA probe with flow cytometry was used to detect the intracellular ROS levels in R28 cells. (D) The intracellular content of ROS was significantly increased by SI, which could be alleviated by MSC coculture. (E) Western blot analyses show the expression of several autophagy protein markers (LAMP2 and LC3B-II). (F) Bars are represented as the mean ± SD of three independent experiments. Represented data are from an individual experiment with three biological replicates. Data are mean ± SD. For original images of the blots, please see the Supplementary Data file.

Journal: International Journal of Medical Sciences

Article Title: Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling

doi: 10.7150/ijms.123975

Figure Lengend Snippet: MSC therapy reversed the SI-induced increased levels of autophagy markers, increased loss of mitochondrial membrane potential, and increased intracellular ROS contents in R28 cells. (A) A dot plot displays the fluorescence density of J-aggregates (y-axis) against JC-1 monomers (x-axis). (B) Quantitative analysis of the loss of MMP by the red and green fluorescence ratio. (C) DCFH-DA probe with flow cytometry was used to detect the intracellular ROS levels in R28 cells. (D) The intracellular content of ROS was significantly increased by SI, which could be alleviated by MSC coculture. (E) Western blot analyses show the expression of several autophagy protein markers (LAMP2 and LC3B-II). (F) Bars are represented as the mean ± SD of three independent experiments. Represented data are from an individual experiment with three biological replicates. Data are mean ± SD. For original images of the blots, please see the Supplementary Data file.

Article Snippet: LC3B-I/II , 1:2000 , Cell Signaling Technology , 2775 , WB.

Techniques: Membrane, Fluorescence, Flow Cytometry, Western Blot, Expressing

Osteogenesis of BMSCs stimulated by DMEM-exo or BMP2-exo. A RNA expression of osteogenesis-related genes (ALP, OPN, OCN, Col-I and OPG). Data were expressed as the mean ± SD for three independent experiments. B Protein expression of early osteoblast differentiation marker (ALP), β-catenin, BMP2, autophagy-related proteins (ATG5, LC3-I, and LC3-II) assessed by Western blot. Data were expressed as the mean ± SD for three independent experiments. The protein levels were quantitated by densitometry quantitation normalized to β-Tubulin. * p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Journal of Orthopaedic Surgery and Research

Article Title: Macrophage-derived exosomal miR-466i-5p and miR-365-2-5p stimulated by BMP-2 promote osteogenesis

doi: 10.1186/s13018-025-06563-9

Figure Lengend Snippet: Osteogenesis of BMSCs stimulated by DMEM-exo or BMP2-exo. A RNA expression of osteogenesis-related genes (ALP, OPN, OCN, Col-I and OPG). Data were expressed as the mean ± SD for three independent experiments. B Protein expression of early osteoblast differentiation marker (ALP), β-catenin, BMP2, autophagy-related proteins (ATG5, LC3-I, and LC3-II) assessed by Western blot. Data were expressed as the mean ± SD for three independent experiments. The protein levels were quantitated by densitometry quantitation normalized to β-Tubulin. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Membranes were incubated overnight at 4 °C with primary antibodies: β-tubulin, ALP (1:1000, ab108337; Abcam); β-catenin (1:1000, ab4074; Abcam); BMP2 (1:1000; ab82511, Abcam); ATG5 (1:1000, Cat. No. 12994; Cell Signaling Technology); and LC3-I/II (1:1000, Cat. No. 2775; Cell Signaling Technology).

Techniques: RNA Expression, Expressing, Marker, Western Blot, Quantitation Assay

Western blot analysis of oxidative stress, apoptosis, and autophagy markers in the liver (A). Mice were treated with vehicle, polimersomes (PS), carbon tetrachloride (CCl 4 ), CCl 4 + berberine (BER), and CCl 4 + BER-PS. Semiquantification of the expression of 4-hydroxynonenal (4-HNE) (B), hem oxygenase-1 (HO-1) (C), cleaved caspase-3 (D), caspase-9 (E), microtubule-associated protein 1 light chain 3 beta (LC3B)-I/II (F), p62 (G), and p21 (H). Each value represents the mean ± SD for 6 mice. *** p < 0.001 CCl 4 compared to control; # p < 0.05, ## p < 0.01, ### p < 0.001 CCl 4 compared to BER + CCl 4 and BER-PS + CCl 4 ; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 BER + CCl 4 compared to BER-PS + CCl 4 .

Journal: Nanoscale Advances

Article Title: Targeted delivery of berberine via ROS-sensitive polymersomes enhances its hepatoprotective activity in CCl 4 -intoxicated mice

doi: 10.1039/d5na00706b

Figure Lengend Snippet: Western blot analysis of oxidative stress, apoptosis, and autophagy markers in the liver (A). Mice were treated with vehicle, polimersomes (PS), carbon tetrachloride (CCl 4 ), CCl 4 + berberine (BER), and CCl 4 + BER-PS. Semiquantification of the expression of 4-hydroxynonenal (4-HNE) (B), hem oxygenase-1 (HO-1) (C), cleaved caspase-3 (D), caspase-9 (E), microtubule-associated protein 1 light chain 3 beta (LC3B)-I/II (F), p62 (G), and p21 (H). Each value represents the mean ± SD for 6 mice. *** p < 0.001 CCl 4 compared to control; # p < 0.05, ## p < 0.01, ### p < 0.001 CCl 4 compared to BER + CCl 4 and BER-PS + CCl 4 ; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 BER + CCl 4 compared to BER-PS + CCl 4 .

Article Snippet: Primary antibodies to extracellular regulated kinase 1/2 (ERK1/2) (#4695), phosphorylated ERK1/2 ( p -ERK1/2 Thr202/Tyr204, #4370), c-Jun N-terminal kinase 1/2 (JNK1/2) (#9252), phosphorylated JNK1/2 ( p -JNK1/2 Thr183/Tyr185, #4668), p38 (#8690), phosphorylated p38 (p-p38 Thr180/Tyr182, #4511), cleaved caspase-3 (#9661), and microtubule-associated protein 1 light chain 3 beta (LC3B)-I/II (#2775) were from Cell Signaling Technologies (Beverly, MA, USA), and GAPDH (HRP-60004) was obtained from Proteintech, (Rosemont, IL, USA).

Techniques: Western Blot, Expressing, Control

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lc3b ii i (Cell Signaling Technology Inc)

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1) Product Images from "Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy"

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