antioxidant molecules Search Results


94
TargetMol antioxidant
PFKL mediates the neuroprotective and <t>antioxidant</t> effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.
Antioxidant, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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95
Chem Impex International carboxyphenol ba
PFKL mediates the neuroprotective and <t>antioxidant</t> effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.
Carboxyphenol Ba, supplied by Chem Impex International, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
SMAC Corp small molecules antioxidant capacity (smac)
PFKL mediates the neuroprotective and <t>antioxidant</t> effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.
Small Molecules Antioxidant Capacity (Smac), supplied by SMAC Corp, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
MultiTarget Pharmaceuticals antioxidant molecules
Natural Antioxidants.
Antioxidant Molecules, supplied by MultiTarget Pharmaceuticals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Forestia Inc small molecules activators of the nrf2-ho-1 antioxidant axis
Natural Antioxidants.
Small Molecules Activators Of The Nrf2 Ho 1 Antioxidant Axis, supplied by Forestia Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Chronomics ltd circulating plasma lipid peroxides, antioxidant enzymes and other small molecules
Natural Antioxidants.
Circulating Plasma Lipid Peroxides, Antioxidant Enzymes And Other Small Molecules, supplied by Chronomics ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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PADMA AG antioxidant molecules
Natural Antioxidants.
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BioMimetic Therapeutics scaffold incorporating angiogenic molecules and antioxidant
The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating <t>antioxidant</t> and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.
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PADMA AG antioxidant molecules like carotenoids, ascorbic acid and terpenoids
The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating <t>antioxidant</t> and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.
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SACRI Antibody small molecule antioxidants
The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating <t>antioxidant</t> and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.
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MitoQ Ltd antioxidant molecule marvel
The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating <t>antioxidant</t> and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.
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MitoQ Ltd triphenylphosphonium ion conjugated to lipophilic antioxidant molecules, such as coenzyme-q
The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating <t>antioxidant</t> and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.
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Image Search Results


PFKL mediates the neuroprotective and antioxidant effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.

Journal: Neural Regeneration Research

Article Title: Hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect neurons from cardiac arrest–induced pyroptosis

doi: 10.4103/NRR.NRR-D-23-01922

Figure Lengend Snippet: PFKL mediates the neuroprotective and antioxidant effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.

Article Snippet: For the second experiment, the cells were divided into five groups that were left untreated or treated with siRNAs, left untreated or treated with 10 μM mitochondria-targeted antioxidant (Mito-TEMPO, TargetMol, Shanghai.

Techniques: Staining, Transplantation Assay, Immunohistochemical staining, Expressing, Immunostaining, Immunofluorescence, ROS Assay, Fluorescence, Analysis, Saline, Immunohistochemistry, Knockdown

Natural Antioxidants.

Journal: Molecules

Article Title: Antioxidant Cardioprotection against Reperfusion Injury: Potential Therapeutic Roles of Resveratrol and Quercetin

doi: 10.3390/molecules27082564

Figure Lengend Snippet: Natural Antioxidants.

Article Snippet: The paradigm of a multitarget therapy based on an association of different antioxidant molecules should be expected to improve the abrogation of oxidative damage and related effects derived from ROS burst, particularly occurring early at the onset of reperfusion.

Techniques: Activity Assay, Membrane, Activation Assay, Inhibition, Expressing

Synthetic antioxidants.

Journal: Molecules

Article Title: Antioxidant Cardioprotection against Reperfusion Injury: Potential Therapeutic Roles of Resveratrol and Quercetin

doi: 10.3390/molecules27082564

Figure Lengend Snippet: Synthetic antioxidants.

Article Snippet: The paradigm of a multitarget therapy based on an association of different antioxidant molecules should be expected to improve the abrogation of oxidative damage and related effects derived from ROS burst, particularly occurring early at the onset of reperfusion.

Techniques: Activation Assay, Activity Assay, Inhibition, Protein-Protein interactions, Binding Assay

Representation of resveratrol cardioprotective effect. Resveratrol activates the Nrf2 signaling pathway, increasing the expression of antioxidant enzymes. It also reduces the expression of pro-apoptotic proteins, such as caspase 3, via the PI3K/Akt pathway. Other effects are the reduction of inflammation and ferroptosis, which has been associated with reduced expression of TNFα, Nf κ B, TfR1, and increased activity of GPX4 after administration of resveratrol. The activation of SIRT1 is related to a decrease in intramitochondrial calcium concentration, which diminishes mitochondrial ROS production.

Journal: Molecules

Article Title: Antioxidant Cardioprotection against Reperfusion Injury: Potential Therapeutic Roles of Resveratrol and Quercetin

doi: 10.3390/molecules27082564

Figure Lengend Snippet: Representation of resveratrol cardioprotective effect. Resveratrol activates the Nrf2 signaling pathway, increasing the expression of antioxidant enzymes. It also reduces the expression of pro-apoptotic proteins, such as caspase 3, via the PI3K/Akt pathway. Other effects are the reduction of inflammation and ferroptosis, which has been associated with reduced expression of TNFα, Nf κ B, TfR1, and increased activity of GPX4 after administration of resveratrol. The activation of SIRT1 is related to a decrease in intramitochondrial calcium concentration, which diminishes mitochondrial ROS production.

Article Snippet: The paradigm of a multitarget therapy based on an association of different antioxidant molecules should be expected to improve the abrogation of oxidative damage and related effects derived from ROS burst, particularly occurring early at the onset of reperfusion.

Techniques: Expressing, Activity Assay, Activation Assay, Concentration Assay

Representation of quercetin cardioprotective effect. Quercetin acts through the inhibition of the enzymes xanthine oxidase, NADPH oxidase and the Fenton reaction, mechanisms leading to a decrease in ROS production. In addition, it acts by activating the selenoprotein TrxR2, which has a powerful antioxidant effect by inactivating ROS. All these mechanisms lead to a decrease in oxidative stress.

Journal: Molecules

Article Title: Antioxidant Cardioprotection against Reperfusion Injury: Potential Therapeutic Roles of Resveratrol and Quercetin

doi: 10.3390/molecules27082564

Figure Lengend Snippet: Representation of quercetin cardioprotective effect. Quercetin acts through the inhibition of the enzymes xanthine oxidase, NADPH oxidase and the Fenton reaction, mechanisms leading to a decrease in ROS production. In addition, it acts by activating the selenoprotein TrxR2, which has a powerful antioxidant effect by inactivating ROS. All these mechanisms lead to a decrease in oxidative stress.

Article Snippet: The paradigm of a multitarget therapy based on an association of different antioxidant molecules should be expected to improve the abrogation of oxidative damage and related effects derived from ROS burst, particularly occurring early at the onset of reperfusion.

Techniques: Inhibition

The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating antioxidant and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.

Journal: Advanced Healthcare Materials

Article Title: Ovarian Function Restoration with Biomimetic Scaffold Incorporating Angiogenic Molecules and Antioxidant in Chemotherapy‐Induced Perimenopausal Model

doi: 10.1002/adhm.202403944

Figure Lengend Snippet: The schematic illustration of hESC‐MPCs laden biomimetic scaffold incorporating antioxidant and angiogenic molecules restorates the chemotherapy‐induced premature ovarian insufficiency in mice. The biomimetic scaffold containing PDRN and melatonin provides higher hESC‐MPCs adhsion, immune moduation, and angiogenesis for ovarian function restoation.

Article Snippet: Baek , D. R. Lee , D. K. Han , Ovarian Function Restoration with Biomimetic Scaffold Incorporating Angiogenic Molecules and Antioxidant in Chemotherapy‐Induced Perimenopausal Model . Adv.

Techniques: