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Image Search Results
Journal: Antioxidants (Basel, Switzerland)
Article Title: Intracellular Polyphenol Wine Metabolites Oppose Oxidative Stress and Upregulate Nrf2/ARE Pathway.
doi: 10.3390/antiox11102055
Figure Lengend Snippet: Figure 4. Dose–response effect of wine extract (WE) and sulforaphane (SFN) on oxidative stress- induced intracellular reactive oxygen species (ROS) formation. (a,b) THP-1 cells and cardiomyocytes were pre-incubated with increasing concentrations (from 200 to 800 µg/mL of total polyphenols) of WE and SFN (1–10 µM) before the addition of tert-butyl hydroperoxide (TBHP, 100 µM). Data represent the mean +/−standard deviation of measurements performed in triplicate in three different experiments; * p < 0.01 increase vs. control; ** p < 0.001 decrease vs. THBP; § p < 0.1 decrease vs. TBHP. (c) Representative flow cytometry analysis of ROS generation induced by TBHP and the inhibitory effect of the highest dose of wine extract. (d) Representative flow cytometry analysis on cell viability of the highest dose of wine extract.
Article Snippet:
Techniques: Incubation, Standard Deviation, Control, Cytometry
Journal: Antioxidants (Basel, Switzerland)
Article Title: Intracellular Polyphenol Wine Metabolites Oppose Oxidative Stress and Upregulate Nrf2/ARE Pathway.
doi: 10.3390/antiox11102055
Figure Lengend Snippet: Figure 5. Wine metabolites activate Nrf2/ARE pathway in basal conditions and in cells exposed to oxidative stress. (a,b) Effect of wine extract (WE) and sulforaphane (SFN) on Nrf2 nuclear translocation. THP-1 cells and cardiomyocytes were pre-incubated with WE, containing 800 µg/mL of total polyphenols and 10 µM SFN with or without the addition of tert-butyl hydroperoxide (TBHP, 100 µM). (c) Effect of WE on mRNA expression of Nrf2 target genes hemeoxygenase-1 (HO-1) and glutamate-cysteine ligase catalytic subunit (GCLC). (d) Average quantification of HO-1 and GCLC protein expression obtained by densitometric analysis and representative Western blot analyses for HO-1 and GCLC protein expression in cardiomyocytes. Data represent the mean +/−standard deviation of measurements performed in triplicate in three different experiments and; * p < 0.01 decrease vs. control; § p < 0.01 increase vs. control; ** p < 0.01 vs. TBHP.
Article Snippet:
Techniques: Translocation Assay, Incubation, Expressing, Western Blot, Standard Deviation, Control
Journal: Scientific reports
Article Title: Unlocking cardiac motion: assessing software and machine learning for single-cell and cardioid kinematic insights.
doi: 10.1038/s41598-024-52081-9
Figure Lengend Snippet: Figure 2. Comparison of the three open-source software programs with in-silico cardiomyocytes with 200% time-to-peak. (a) The first experiment with “grey” patterned cardiomyocyte. The plot on the left side of the panel represents the speed profile evaluated by the three software programs. The grey profile is the benchmark considered in this study (MUSCLEMOTION), the cyan profile derives from CONTRACTIONWAVE evaluation, and the orange profile is the ViKiE estimation. The histograms on the right side represent the four parameters extracted by the profiles and measured by the three methodologies. (b) The second experiment with “fog” patterned cardiomyocyte. As in panel (a), the profiles and histograms of the software evaluations are reported to address the ground-truth comparison.
Article Snippet: On the 26th day of culture, the cells were purified from all non-cardiomyocytes by
Techniques: Comparison, Software, In Silico
Journal: Frontiers in Pharmacology
Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity
doi: 10.3389/fphar.2022.863322
Figure Lengend Snippet: OEA inhibited DOX-induced oxidative stress and apoptosis in cardiomyocytes through TRPV1 pathway. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM), GW6471 (5 μM), capsazepine (10 μM), nonivamide (10 μM), fenofibrate (100 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. Levels of (A) GST (B) TBARS and (C) cell viability was assessed in HL-1 cardiomyocytes. (D) TUNEL positive cells shown in (E) were counted. (E) TUNEL staining of HL-1 cardiomyocytes. Data are expressed as mean ± SEM, n = 4. ***, p < 0.001 vs. control. ##, p < 0.01; ###, p < 0.001 vs. DOX + vehicle. $$$, p < 0.001 vs. DOX + OEA.
Article Snippet: Adult derived primary
Techniques: TUNEL Assay, Staining, Control
Journal: Frontiers in Pharmacology
Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity
doi: 10.3389/fphar.2022.863322
Figure Lengend Snippet: OEA promotes TRPV1-mediated PI3K/ Akt signaling in cardiomyocytes. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM), GW6471 (5 μM), capsazepine (10 μM) and nonivamide (10 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. PI3K, Akt, p-PI3K and p-Akt was determined using western blot analysis.
Article Snippet: Adult derived primary
Techniques: Western Blot
Journal: Frontiers in Pharmacology
Article Title: Oleoylethanolamide as a New Therapeutic Strategy to Alleviate Doxorubicin-Induced Cardiotoxicity
doi: 10.3389/fphar.2022.863322
Figure Lengend Snippet: Inhibition of the PI3K-Akt signaling blocks the protective effects of OEA in cardiomyocytes. HL-1 cells were treated with 0.1% DMSO, OEA (30 μM) and LY294002 (10 μM) for 30 min. Cells were then treated with DOX (2 μM) for 24 h. Levels of (A) GST (B) TBARS and (C) cell viability was assessed in HL-1 cardiomyocytes. (D) TUNEL positive cells shown in (F) were counted. (E) Fluorescence quantification for caspase three in (G) were calculated. (F) TUNEL staining of HL-1 cardiomyocytes. (G) Immunofluorescence staining of caspase three in HL-1 cardiomyocytes. Data are expressed as mean ± SEM, n = 4. ***, p < 0.001 vs. control. #, p < 0.05; ##, p < 0.01; ###, p < 0.001 vs. DOX + vehicle. $, p < 0.05; $$, p < 0.01; $$$, p < 0.001 vs. DOX + OEA.
Article Snippet: Adult derived primary
Techniques: Inhibition, TUNEL Assay, Fluorescence, Staining, Immunofluorescence, Control
Journal: Journal of Cardiovascular Development and Disease
Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels
doi: 10.3390/jcdd13070339
Figure Lengend Snippet: Anaesthesia device and airtight chamber system used during 5.1% sevoflurane exposure of cardiomyocyte cells.
Article Snippet: Human Cardiomyocyte Complete Media with Serum,
Techniques:
Journal: Journal of Cardiovascular Development and Disease
Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels
doi: 10.3390/jcdd13070339
Figure Lengend Snippet: ( A , B ) The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on cytosolic calcium levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM, on the 20th cycle) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 3). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM group.
Article Snippet: Human Cardiomyocyte Complete Media with Serum,
Techniques: Control
Journal: Journal of Cardiovascular Development and Disease
Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels
doi: 10.3390/jcdd13070339
Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on apoptosis levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.005 and d p ˂ 0.001 vs. REM, and e p ˂ 0.05 vs. SEV + REM.
Article Snippet: Human Cardiomyocyte Complete Media with Serum,
Techniques: Control
Journal: Journal of Cardiovascular Development and Disease
Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels
doi: 10.3390/jcdd13070339
Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on reactive oxygen and mitochondrial depolarisation levels in cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 and b p ˂ 0.05 vs. control, c p ˂ 0.001 vs. SEV, e p ˂ 0.001 and f p ˂ 0.05 vs. REM, and g p ˂ 0.001 vs. SEV + REM.
Article Snippet: Human Cardiomyocyte Complete Media with Serum,
Techniques: Control
Journal: Journal of Cardiovascular Development and Disease
Article Title: The Mitigating Effect of Remifentanil Against Sevoflurane-Induced Cardiotoxicity in Human Cardiomyocytes via TRPA1 Channels
doi: 10.3390/jcdd13070339
Figure Lengend Snippet: The effect of sevoflurane (SEV, 5.1%, 6 h) and remifentanil (REM, 2.5 µM, 30 min) on caspase-3 and caspase-9 levels in the cardiomyocyte cells. Cells were stimulated by cinnamaldehyde (CIN, 0.1 mM for 10 min) but were inhibited by AP18 (0.1 mM for 30 min) (mean ± SD, n = 10). a p ˂ 0.001 vs. control, b p ˂ 0.001 vs. SEV, c p ˂ 0.001 vs. REM, and d p ˂ 0.001 vs. SEV + REM.
Article Snippet: Human Cardiomyocyte Complete Media with Serum,
Techniques: Control
Journal: International Journal of Nanomedicine
Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application
doi: 10.2147/IJN.S34574
Figure Lengend Snippet: Addition of CNF to the PLGA substrate alters the topography of the material. Using an Asylum MFP three-dimensional atomic force microscope (scan rate 1.0 Hz, AC mode with 256 × 256 scan points and lines), ( A ) CNF are shown for a 25:75 ratio (PLGA:CNF [wt%:wt%]) sample with a PLGA density of 0.025 g/mL which increases surface nanometer features as well as the total substrate surface area as compared with an etched glass cover slip. ( B ) It is shown for all PLGA:CNF ratio samples that increasing the CNF weight ratio increased the surface area of the substrate by creating nano, submicron, and micron features. ( C ) By normalizing the protein adsorption OD readings to the lowest reading (ie, for the controlled etched glass coverslip) and comparing it with the surface area percent increase, the results indicate that protein saturation was around 40%–55% of amount of increase of the surface area, and provide evidence that increasing the surface area (through addition of CNF) allows more proteins to attach to the surface to promote cell attachment. ( D ) Calculating the normalized protein adsorption capacity indicates that the 75:25 and 50:50 ratios (PLGA:CNF [wt%:wt%]) had the highest ability to attach the most proteins to a particular surface, indicating that one of the mechanisms regulating cardiomyocyte interactions is increasing material protein capacity through altering topographical features by addition of CNF. Notes: This is evident in the similar cardiomyocyte growth trends reported by Stout et al. * P < 0.05 CNF wt% in materials versus 0% CNF wt% in materials; ** P < 0.05 CNF wt% in materials versus 75% CNF wt% in materials; *** P < 0.05 CNF wt% in materials versus 50% CNF wt% in materials; **** P < 0.05 CNF wt% in materials versus 75% CNF wt% in materials, and ***** P < 0.05 CNF wt% in materials versus 100% CNF wt% in materials. Data are shown as the mean count of n = 3. Abbreviations: CNF, carbon nanofibers; OD, optical density; PLGA, poly(lactic-co-glycolic-acid).
Article Snippet: Cells were seeded into 12-well
Techniques: Microscopy, Adsorption, Cell Attachment Assay
Journal: International Journal of Nanomedicine
Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application
doi: 10.2147/IJN.S34574
Figure Lengend Snippet: Cardiomyocyte cell proliferation on a PLGA density of 0.025 g/mL after ( A ) 24, ( B ) 72, and ( C ) 120 hours on 100 nm diameter PLGA:CNF composite materials of interest in this study. Notes: Seeding density was 5 × 104 cells/cm 2 . Data are shown as the mean count of n = 3. The control was the glass substrate. * P < 0.05 versus control; ** P < 0.05 versus similar PLGA:CNF composite ratios and different densities; *** P < 0.05 versus similar PLGA:CNF composite ratios between 24 and 72 hours, and **** P < 0.05 versus PLGA:CNF composite ratios between 72 and 120 hours. Abbreviations: CNF, carbon nanofibers; PLGA, poly(lactic-co-glycolic-acid).
Article Snippet: Cells were seeded into 12-well
Techniques: Control
Journal: International Journal of Nanomedicine
Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application
doi: 10.2147/IJN.S34574
Figure Lengend Snippet: Immunofluorescence staining for cardiomyocyte biomarkers on a 0.025 g/mL PLGA density PLGA:CNF composite after 120 hours of incubation. ( A ) Cardiac troponin T (green) biomarker with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample. ( B ) Connexin-43 (red) with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample. ( C ) α-SCA (yellow) with DAPI stain (blue) on a 50:50 (PLGA:CNF [wt%:wt%]) sample within the cardiomyocytes, indicating cardiomyocyte activity on the materials. Seeding density was 5.5 × 10 4 cells/mL. Scale bar 200 μm. Area fraction (%), area of stain on the surface compared with the total area of image, of DAPI (nucleus) and ( B ) cardiac troponin T, ( D ) connexin-43, and ( F ) α-SCA after 120 hours of cell incubation, on all PLGA:CNF (wt%:wt%) ratio samples. Notes: The results indicate trends similar to those of the adhesion and proliferation experiments , thus verifying those results and indicating cardiomyocyte activity on the materials. Seeding density was 5.5 × 10 4 cells/mL. Data are shown as the mean count of n = 3. Control was glass substrate. * P < 0.05 versus 100:0 (PLGA:CNF [wt%:wt%]) ratio sample; ** P < 0.05 versus 75:25 (PLGA:CNF [wt%:wt%]) ratio sample; *** P < 0.05 versus 50:50 (PLGA:CNF [wt%:wt%]) ratio sample; **** P < 0.05 versus 25:75 (PLGA:CNF [wt%:wt%]) ratio sample; ***** P < 0.05 versus 0:100 (PLGA:CNF [wt%:wt%]) ratio sample, and ****** P < 0.05 versus control sample. Abbreviations: CNF, carbon nanofibers; cTNT, cardiac Troponin-T; PLGA, poly(lactic-co-glycolic-acid).
Article Snippet: Cells were seeded into 12-well
Techniques: Immunofluorescence, Staining, Incubation, Biomarker Discovery, Activity Assay, Control
Journal: International Journal of Nanomedicine
Article Title: Mechanisms of greater cardiomyocyte functions on conductive nanoengineered composites for cardiovascular application
doi: 10.2147/IJN.S34574
Figure Lengend Snippet: Schematic illustration, with a three-dimensional atomic force microscopy topographical image (scan rate 1.0 Hz, AC mode with a 256 × 256 scan points and lines), of the proposed mechanism by which PLGA:CNF materials may be superior to conventional materials for cardiovascular application. The bioactive surfaces of PLGA:CNF mimic those of the natural myocardium (in stiffness) and increasing protein adsorption capacitance to promote greater amounts of protein adsorption ( A ) and efficiently stimulate cardiomyocyte growth better than conventional materials and plain nanorough surfaces ( B and C ). ( A ) Once a patch is placed into its host, protein adsorption begins on substrates immediately. ( B ) Cardiomyocyte attachment and growths begins. ( C ) Due to mimicking the native myocardium (in stiffness) and ability to increase protein adsorption capacitance, more cardiomyocytes adhere and grow on nanorough stiff material as compared with conventional and plain nanorough materials. Abbreviations: CNF, carbon nanofibers; PLGA, poly(lactic-co-glycolic-acid).
Article Snippet: Cells were seeded into 12-well
Techniques: Microscopy, Adsorption
Journal: Cells
Article Title: Dual Roles of Plasma miRNAs in Myocardial Injuries After Polytrauma: miR-122-5p and miR-885-5p Reflect Inflammatory Response, While miR-499a-5p and miR-194-5p Contribute to Cardiomyocyte Damage.
doi: 10.3390/cells14040300
Figure Lengend Snippet: Figure 3. Both polytrauma cocktail and LPS + nigericin stimulations lead to an upregulation of miR-885-5p and miR-122-5p expression in HCM cells. (A) HCM cells were treated with a poly- trauma cocktail (PTC) containing C3a, C5a, IL-1β, IL-6, IL-8, and TNF-α for 4 h. miRNAs were isolated, and RT-qPCR was performed to assess the expression levels of miR-885-5p, miR-122-5p, miR-194-5p, miR-424-5p, and miR-499a-5p in non-treated (control) or treated HCM cells. (B) HCM cells were stimulated with LPS for 4 h, followed by nigericin stimulation in serum-free medium for 1 h (LPS + nigericin). miRNA was isolated, and RT-qPCR was used to evaluate the expression levels of miR-885-5p, miR-122-5p, miR-194-5p, miR-424-5p, and miR-499a-5p in non-treated (control) or treated HCM cells. * p < 0.05, ns = no significance.
Article Snippet: Cell Culture and
Techniques: Expressing, Isolation, Quantitative RT-PCR, Control