Journal: International journal of medical sciences

Article Title: P66Shc is increased in peripheral blood mononuclear cells of the patients with obstructive sleep apnea.

doi: 10.7150/ijms.80343

Figure Lengend Snippet: Figure 2. P66Shc mRNA levels (n=73) were positively correlated with (A) plasma 3-NT, (B) oxLDL, and (C) AOPP levels by Spearman’s rank correlation coefficient.

Article Snippet: Enzyme-linked Immunosorbent Assay The level of plasma 3-NT (Elabscience, Catalog#E-EL-0040c, China), oxLDL (Elabscience, Catalog#E-EL-H6021, China) and AOPP (Abbkine, Catalog#KTB1060, China) were detected with the enzyme-linked immunosorbent assay (ELISA) commercial kits according to the recommendations of the manufacturers.

Techniques: Clinical Proteomics

Journal: Drug Design, Development and Therapy

Article Title: Baolier Capsule’s Secret Weapon: Piperine Boosts Cholesterol Excretion to Combat Atherosclerosis

doi: 10.2147/DDDT.S499598

Figure Lengend Snippet: Key Resources Table

Article Snippet: LDL-C assay kit , Elabscience , E-BC-K205-M.

Techniques: Control, shRNA, Sequencing, Staining, Fluorescence, Microscopy, AST Assay, Phospholipid Assay, Mass Spectrometry

Journal: Redox Biology

Article Title: Folic acid modulates VPO1 DNA methylation levels and alleviates oxidative stress-induced apoptosis in vivo and in vitro

doi: 10.1016/j.redox.2018.08.005

Figure Lengend Snippet: The effect of folic acid on reactive oxygen species (ROS) and 8-Hydroxydeoxyguanosine (8-OHdG) level in HUVECs. HUVCE were treated with 0–1000 nmol/L folic acid for 48 h and exposed to 120 μg/mL ox-LDL for the first 24 h. (A) The intracellular ROS was measured by flow cytometry using DCFH-DA staining. The peaks in each panel represent the mean fluorescence intensities. (B) Representative images of unirradiated and irradiated cells obtained by the ImageStream. (C) ROS levels are reported as DCF Florescence, which means percentage of control group cells. (D) Intracellular 8-OHdG level was assayed by ELISA. The plotted values are mean ± SE values for 3 independent experiments. a, p < 0.05 compared with the ox-LDL + FA20. b, p < 0.05 compared with the ox-LDL + FA0.

Article Snippet: The plasma ox-LDL concentration was detected using the mouse ox-LDL ELISA Kit (CUSABIO TECHNOLOGY, Wuhan, China) according to the manufacturer's instructions.

Techniques: Flow Cytometry, Staining, Fluorescence, Irradiation, Control, Enzyme-linked Immunosorbent Assay

Journal: Cardiovascular diabetology

Article Title: Klotho inhibits renal ox-LDL deposition via IGF-1R/RAC1/OLR1 signaling to ameliorate podocyte injury in diabetic kidney disease.

doi: 10.1186/s12933-023-02025-w

Figure Lengend Snippet: Fig. 6 Klotho regulated podocytic ox-LDL deposition via IGF-1R/RAC1/OLR1 signal axis. A IF analysis of the expression of Nephrin and RAC1 following administration of the inhibitor (PPP) and agonist (IGF2) of IGF-1R on KL+/− DKD and TgKL DKD, respectively. B Western blot analysis was conducted to determine the expression of RAC1, Podocin, and Cleaved Caspase3 following administration of the inhibitor (PPP) and agonist (IGF2) of IGF-1R on KL+/− DKD and TgKL DKD, respectively. C Representative western blot and summarized data showing the effects of administration of the inhibitor (PPP) and agonist (IGF2) of IGF-1R in the absence or presence of Klotho on the relative protein levels of OLR1, RAC1, Podocin, WT1 and Cleaved Caspase3. *P < 0.05; **P < 0.01; ***P < 0.001

Article Snippet: The antibodies used were listed below: anti-ox-LDL antibody (1:100, orb10973, Biorybt), anti-Podocin antibody (1:200, PA5-79757, Invitrogen), anti-Klotho antibody (1:100, PA5-88303, Invitrogen), anti-WT1 antibody (1:50, ab89901, Abcam), anti-PDGFRβ antibody (1:50, ab89901, Abcam), anti-GATA3 antibody (1:2400, ab199428, Abcam), anti-CXCL16 antibody (1:200, 60123- 1-Ig, Proteintech), anti-Parkin antibody (1:100, YT3593, ImmunoWay), anti-RAC1 antibody (1:20, AF385-SP, R&D), anti-Nephrin antibody (1:10, sc-376522, Santa Cruz), anti-OLR1 antibody (1:100, 11837-1-AP, Proteintech), anti-SYNPO antibody (1:200, 21064-AP, Proteintech), anti-IGF-1R antibody (1:10, sc-81464, Santa Cruz), goat polyclonal secondary antibody to mouse Alexa fluor 488 (1:400, ab150113, Abcam), goat polyclonal secondary antibody to rabbit Alexa fluor 555 (1:400, ab150078, Abcam), goat polyclonal secondary antibody to rabbit Alexa fluor 647 (1:400, ab150079, Abcam), goat antimouse Alexa fluor 568 (1:400, ab175473, Abcam), DAPI (1:1000, C1002, Beyotime).

Techniques: Expressing, Western Blot

Journal: Nutrients

Article Title: Systemic and Retinal Protective Effects of Butyrate in Early Type 2 Diabetes via Gut Microbiota–Lipid Metabolism Interaction

doi: 10.3390/nu17142363

Figure Lengend Snippet: High-fat diet-induced serum lipid disorders that were reduced by butyrate diet: ( A ) CHOL (cholesterol), ( B ) LDL-C (low-density lipoprotein cholesterol), ( C ) HDL-C (high-density lipoprotein cholesterol), ( D ) TG (triglyceride), ( E ) ApoA1 (apolipoprotein A1), ( F ) ApoB (apolipoprotein B), ( G ) ApoE (apolipoprotein E), and ( H ) Lp (lipoprotein) levels were measured in the four groups ( n = 4 mice per group, one-way ANOVA test).* p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: Immunohistochemical (IHC) staining was performed on both liver and retinal sections using primary antibodies against HMG-CoA reductase (HMGCR, 1:250 dilution, 13533-1-AP, Proteintech, Wuhan, China) and a low-density lipoprotein receptor (LDLR, 1:250 dilution, 10785-1-AP, Proteintech).

Techniques:

Journal: Nutrients

Article Title: Systemic and Retinal Protective Effects of Butyrate in Early Type 2 Diabetes via Gut Microbiota–Lipid Metabolism Interaction

doi: 10.3390/nu17142363

Figure Lengend Snippet: Butyrate protects the retina and enhances cholesterol metabolism in the retinas of type 2 diabetic mice. ( A ) Representative hematoxylin and eosin staining images illustrate the retinal structure across the four groups. Scale bar: 50 μm. ( B ) Representative immunohistochemistry images display retinal HMGCR expression in the four groups. ( C ) Representative immunofluorescence images show retinal LDLR expression in the four groups. ( D ) Quantitative analysis of retinal thickness in the four groups ( n = 4 mice with 2 fields per mouse, one-way ANOVA test). ( E ) Quantification of mean HMGCR expression intensity in the inner retinal segments ( n = 4 mice with 3 fields per mouse, one-way ANOVA test). ( F ) Quantification of mean LDLR expression intensity in the inner retinal segments ( n = 4 mice with 3 fields per mouse, one-way ANOVA test). Scale bar: 50 μm. Ns: not significant, **** p < 0.0001.

Article Snippet: Immunohistochemical (IHC) staining was performed on both liver and retinal sections using primary antibodies against HMG-CoA reductase (HMGCR, 1:250 dilution, 13533-1-AP, Proteintech, Wuhan, China) and a low-density lipoprotein receptor (LDLR, 1:250 dilution, 10785-1-AP, Proteintech).

Techniques: Staining, Immunohistochemistry, Expressing, Immunofluorescence

Journal: Frontiers in Cardiovascular Medicine

Article Title: Hematopoietic Cell-Specific SLC37A2 Deficiency Accelerates Atherosclerosis in LDL Receptor-Deficient Mice

doi: 10.3389/fcvm.2021.777098

Figure Lengend Snippet: SLC37A2 deficiency promotes oxidized LDL (OxLDL)-induced macrophage inflammation in vitro . (A) SLC37A2 protein expression analyzed by Western blotting in WT and Slc37a2 −/− bone marrow-derived macrophages (BMDMs) treated with 50 μg/ml oxLDL for 0-24 h. (B) Quantification of cellar total cholesterol (TC), free cholesterol (FC), and cholesterol ester (CE) in WT and Slc37a2 −/− BMDMs after treated with or without 25 or 50 μg/ml oxLDL for 24 h. (C) Relative transcript level of cytokines in WT and Slc37a2 −/− BMDMs stimulated with 50 μg/ml oxLDL for 0-24 h, measured by qPCR. Data are representative of two independent experiments with three samples per group (mean ± SEM). * p < 0.05; unpaired, two-tailed Student's t -test.

Article Snippet: To induce foam cell formation, BMDMs were treated with 25 or 50 μg/ml oxLDL (Athens Research & Technology) for 0-24 h. In some experiments, BMDMs were pretreated for 30 min with hexokinase inhibitor 2-deoxy-D-glucose (2-DG; 10 mM, Sigma-Aldrich), actin polymerization inhibitor cytochalasin D (10 μM, Cayman), or fatty acid β-oxidation inhibitor etomoxir (50 μM, Cayman) and subsequently treated with apoptotic cells for an additional 4 h in the presence of each inhibitor.

Techniques: In Vitro, Expressing, Western Blot, Derivative Assay, Two Tailed Test