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n methyl d aspartic acid nmda  (Millipore)
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Millipore n methyl d aspartic acid nmda
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
N Methyl D Aspartic Acid Nmda, supplied by Millipore, 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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n methyl d aspartic acid nmda  (Selleck Chemicals)
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Selleck Chemicals n methyl d aspartic acid nmda
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
N Methyl D Aspartic Acid Nmda, supplied by Selleck Chemicals, 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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nmda receptor agonist n methyl d aspartic acid  (Millipore)
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Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
Nmda Receptor Agonist N Methyl D Aspartic Acid, supplied by Millipore, 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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n methyl d aspartic acid  (Millipore)
86
Millipore n methyl d aspartic acid
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
N Methyl D Aspartic Acid, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/n methyl d aspartic acid/product/Millipore
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p n methyl d aspartic acid receptor nmdar 2b  (Cell Signaling Technology Inc)
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Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
P N Methyl D Aspartic Acid Receptor Nmdar 2b, supplied by Cell Signaling Technology 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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brain iron accumulation nm normetanephrine nmda n methyl d aspartate acid  (Neurogeneration)
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Neurogeneration brain iron accumulation nm normetanephrine nmda n methyl d aspartate acid
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
Brain Iron Accumulation Nm Normetanephrine Nmda N Methyl D Aspartate Acid, supplied by Neurogeneration, 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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n methyl d aspartic acid nmda  (Tocris)
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Tocris n methyl d aspartic acid nmda
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
N Methyl D Aspartic Acid Nmda, supplied by Tocris, 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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n methyl d aspartic acid nmda - by Bioz Stars, 2024-10
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n‑methyl‑d‑aspartic acid nmda  (Millipore)
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Millipore n‑methyl‑d‑aspartic acid nmda
Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and <t>NMDA-induced</t> oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, <t>N-Methyl-D-aspartic</t> acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.
N‑Methyl‑D‑Aspartic Acid Nmda, supplied by Millipore, 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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Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and NMDA-induced oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, N-Methyl-D-aspartic acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.

Journal: International Journal of Molecular Medicine

Article Title: Triptonide protects retinal cells from oxidative damage via activation of Nrf2 signaling

doi: 10.3892/ijmm.2024.5400

Figure Lengend Snippet: Tn reduces the expression of inflammatory cytokines and increases oxidative stress-related genes in light-induced and NMDA-induced oxidative stress models. (A-C) In the NMDA-induced models stimulating oxidative stress, Nrf2 and antioxidant response element-dependent genes HO1 and NQO1 increased, which further increased in Tn pretreatment groups. (D and E) Reverse transcription-quantitative PCR assays of retinal inflammatory cytokines were reduced after Tn pretreatment in the light and NMDA-induced oxidative stress models. (F) In the light and NMDA-induced oxidative stress models, Tn significantly increased the levels of Nrf2, HO1 and NQO1 protein expression, and similarly inhibited the protein expression of retinal inflammatory cytokines. (G and H) Similarly, HO1 and NQO1 anti-oxidative genes were reduced in Tn pretreatment group. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005. (n=5). Tn, triptonide; NMDA, N-Methyl-D-aspartic acid; Nrf2, nuclear factor erythrocyte 2-related factor 2; HO1, heme oxygenase-1; NQO1, NAD(P)H: quinone oxidoreductase 1; Ctrl, control; GPX1, glutamine peroxidase 1; GSS, glutathione synthetase; GST, glutathione S-transferase; SOD2, superoxide dismutase 2.

Article Snippet: Tn and N-Methyl-D-aspartic acid (NMDA) were obtained from Sigma-Aldrich; Merck KGaA.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

Tn ameliorates retinal structure and functions in light-induced and NMDA-induced oxidative stress models of mice retina. (A and B) H&E staining showed the reduced thickness of retina ONL in the NMDA- and light-induced oxidative damage models. Tn pretreatment successfully reduced ONL thickness reduction. (C and D) TUNEL (green) was measured by fluorescence, showing the number of retinal cells undergoing apoptosis. (E and F) NeuN (red) was used to label retinal ganglion cells. (G) Electroretinographies reflect the function of retinal nerve electrophysiology, and a-wave and b-wave amplitude was quantified and analyzed. (H and I) Bar plot showing the changes in a-wave and b-wave amplitudes. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005 (n=5). Scale bar, 100 μ m. Tn, triptonide; ONL, outer nuclear layer; NMDA, N-Methyl-D-aspartic acid; TUNEL, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling; Ctrl, control.

Journal: International Journal of Molecular Medicine

Article Title: Triptonide protects retinal cells from oxidative damage via activation of Nrf2 signaling

doi: 10.3892/ijmm.2024.5400

Figure Lengend Snippet: Tn ameliorates retinal structure and functions in light-induced and NMDA-induced oxidative stress models of mice retina. (A and B) H&E staining showed the reduced thickness of retina ONL in the NMDA- and light-induced oxidative damage models. Tn pretreatment successfully reduced ONL thickness reduction. (C and D) TUNEL (green) was measured by fluorescence, showing the number of retinal cells undergoing apoptosis. (E and F) NeuN (red) was used to label retinal ganglion cells. (G) Electroretinographies reflect the function of retinal nerve electrophysiology, and a-wave and b-wave amplitude was quantified and analyzed. (H and I) Bar plot showing the changes in a-wave and b-wave amplitudes. Data are expressed as the mean ± standard error of the mean. * P<0.05, ** P<0.01 and *** P<0.005 (n=5). Scale bar, 100 μ m. Tn, triptonide; ONL, outer nuclear layer; NMDA, N-Methyl-D-aspartic acid; TUNEL, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling; Ctrl, control.

Article Snippet: Tn and N-Methyl-D-aspartic acid (NMDA) were obtained from Sigma-Aldrich; Merck KGaA.

Techniques: Staining, TUNEL Assay, Fluorescence, End Labeling, Control