antibodies against superoxide dismutase 2 sod2  (Boster Bio)


Bioz Verified Symbol Boster Bio is a verified supplier
Bioz Manufacturer Symbol Boster Bio manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94

    Structured Review

    Boster Bio antibodies against superoxide dismutase 2 sod2
    RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and <t>SOD2</t> are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P
    Antibodies Against Superoxide Dismutase 2 Sod2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against superoxide dismutase 2 sod2/product/Boster Bio
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    antibodies against superoxide dismutase 2 sod2 - by Bioz Stars, 2022-10
    94/100 stars

    Images

    1) Product Images from "Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones"

    Article Title: Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/4345037

    RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and SOD2 are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P
    Figure Legend Snippet: RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and SOD2 are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P

    Techniques Used: Expressing, Immunohistochemistry, Mouse Assay

    2) Product Images from "H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway"

    Article Title: H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway

    Journal: EBioMedicine

    doi: 10.1016/j.ebiom.2019.10.059

    H19 facilitated CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19 or rAAV-vector injected CaOx nephrocalcinosis mouse models (Magnification, × 200). (c) Western blot analysis was performed to detect HMGB1, TLR4, p-NF-kB and NF-kB protein expression in H19-treated kidney tissue. GAPDH served as an internal control. (d) qRT-PCR analysis was performed to detect the expression levels of proinflammatory cytokines in kidney tissue. The data are shown as the mean ± standard deviation (SD) of three independent experiments. (* P
    Figure Legend Snippet: H19 facilitated CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19 or rAAV-vector injected CaOx nephrocalcinosis mouse models (Magnification, × 200). (c) Western blot analysis was performed to detect HMGB1, TLR4, p-NF-kB and NF-kB protein expression in H19-treated kidney tissue. GAPDH served as an internal control. (d) qRT-PCR analysis was performed to detect the expression levels of proinflammatory cytokines in kidney tissue. The data are shown as the mean ± standard deviation (SD) of three independent experiments. (* P

    Techniques Used: In Vivo, Light Microscopy, Staining, Immunohistochemistry, Expressing, Plasmid Preparation, Injection, Western Blot, Quantitative RT-PCR, Standard Deviation

    miR-216b reversed the effect of H19 on CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . (a) CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19-, miR-216b agonist-, or combination-treated CaOx nephrocalcinosis mouse models (magnification in all panels is 200 ×). Quantifications were performed using ImageJ. The data are shown as the mean ± SD of three independent experiments. (* P
    Figure Legend Snippet: miR-216b reversed the effect of H19 on CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . (a) CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19-, miR-216b agonist-, or combination-treated CaOx nephrocalcinosis mouse models (magnification in all panels is 200 ×). Quantifications were performed using ImageJ. The data are shown as the mean ± SD of three independent experiments. (* P

    Techniques Used: In Vivo, Light Microscopy, Staining, Immunohistochemistry, Expressing

    3) Product Images from "Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation"

    Article Title: Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation

    Journal: Scientific Reports

    doi: 10.1038/srep30146

    p38 activation leads to augmented oxidative stress in offspring of LPS-treated mothers after isoproterenol treatment and schematic illustration of the current study. Offspring were treated as described in Fig. 6 . ( a,b ) The mRNA levels of Nox2, Nox4, p67 phox , p47 phox , p22 phox ( a ) and Sod1, Sod2, Sod3 , catalase , Gpx1 ( b ) in left ventricle were determined by real-time RT-PCR. β-actin was taken as internal control. n = 5 offspring in each group. Error bar represents S.D. * p
    Figure Legend Snippet: p38 activation leads to augmented oxidative stress in offspring of LPS-treated mothers after isoproterenol treatment and schematic illustration of the current study. Offspring were treated as described in Fig. 6 . ( a,b ) The mRNA levels of Nox2, Nox4, p67 phox , p47 phox , p22 phox ( a ) and Sod1, Sod2, Sod3 , catalase , Gpx1 ( b ) in left ventricle were determined by real-time RT-PCR. β-actin was taken as internal control. n = 5 offspring in each group. Error bar represents S.D. * p

    Techniques Used: Activation Assay, Quantitative RT-PCR

    Increased NADPH oxidase contributes to an imbalance of ROS generation and elimination in offspring from LPS-treated mothers after isoproterenol treatment. Offspring were treated as describe in Fig. 1 . ( a ) The mRNA levels and protein levels of ROS generation related genes (NADPH oxidase subunit, such as Nox2, Nox4, p67 phox , p47 phox and p22 phox ) in left ventricle were determined by real-time RT-PCR or immunoblotting, respectively. n = 5 offspring in each group. ( b ) The mRNA levels and protein levels of ROS elimination related genes (antioxidant enzymes, such as Sod1, Sod2, Sod3, catalase and Gpx1 ) in left ventricle were determined by real-time RT-PCR and immunoblotting, respectively. β-actin was taken as internal control in real-time RT-PCR. Representative plots in each group and statistical data of relative densitometry, normalized by GAPDH, are shown. n = 5 offspring in each group. Error bar represents S.D. * p
    Figure Legend Snippet: Increased NADPH oxidase contributes to an imbalance of ROS generation and elimination in offspring from LPS-treated mothers after isoproterenol treatment. Offspring were treated as describe in Fig. 1 . ( a ) The mRNA levels and protein levels of ROS generation related genes (NADPH oxidase subunit, such as Nox2, Nox4, p67 phox , p47 phox and p22 phox ) in left ventricle were determined by real-time RT-PCR or immunoblotting, respectively. n = 5 offspring in each group. ( b ) The mRNA levels and protein levels of ROS elimination related genes (antioxidant enzymes, such as Sod1, Sod2, Sod3, catalase and Gpx1 ) in left ventricle were determined by real-time RT-PCR and immunoblotting, respectively. β-actin was taken as internal control in real-time RT-PCR. Representative plots in each group and statistical data of relative densitometry, normalized by GAPDH, are shown. n = 5 offspring in each group. Error bar represents S.D. * p

    Techniques Used: Quantitative RT-PCR

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Boster Bio antibodies against superoxide dismutase 2 sod2
    RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and <t>SOD2</t> are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P
    Antibodies Against Superoxide Dismutase 2 Sod2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against superoxide dismutase 2 sod2/product/Boster Bio
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    antibodies against superoxide dismutase 2 sod2 - by Bioz Stars, 2022-10
    94/100 stars
      Buy from Supplier

    Image Search Results


    RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and SOD2 are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Identification of Resolvin D1 and Protectin D1 as Potential Therapeutic Agents for Treating Kidney Stones

    doi: 10.1155/2022/4345037

    Figure Lengend Snippet: RvD1 and PD1 reduced kidney injury by inhibiting oxidative damage. (a) Treatment with different concentrations of RvD1 (18.75 and 31.25 μ g/kg) and PD1 (11.25 and 18.75 μ g/kg) in the CaOx deposition mouse model. Representative plots showing NOX2 and SOD2 are presented (×200; scale bar: 20 μ m). Intracellular ROS levels were measured by the DHE method (×200; scale bar: 20 μ m). (b–d) The ratio of the areas with positive expression of NOX2, SOD2, and DHE, as determined by IHC. One representative plot of n = 5 mice is shown. # P

    Article Snippet: For immunohistochemical staining, the slices were incubated with primary antibodies against superoxide dismutase 2 (SOD2) (1 : 800, Boster, BM4813) and NADPH oxidase 2 (NOX2) (1 : 200, Boster, BA2811) overnight at 4°C and then visualized by an Envision HRP Polymer system (Boster, Wuhan, China).

    Techniques: Expressing, Immunohistochemistry, Mouse Assay

    H19 facilitated CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19 or rAAV-vector injected CaOx nephrocalcinosis mouse models (Magnification, × 200). (c) Western blot analysis was performed to detect HMGB1, TLR4, p-NF-kB and NF-kB protein expression in H19-treated kidney tissue. GAPDH served as an internal control. (d) qRT-PCR analysis was performed to detect the expression levels of proinflammatory cytokines in kidney tissue. The data are shown as the mean ± standard deviation (SD) of three independent experiments. (* P

    Journal: EBioMedicine

    Article Title: H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway

    doi: 10.1016/j.ebiom.2019.10.059

    Figure Lengend Snippet: H19 facilitated CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19 or rAAV-vector injected CaOx nephrocalcinosis mouse models (Magnification, × 200). (c) Western blot analysis was performed to detect HMGB1, TLR4, p-NF-kB and NF-kB protein expression in H19-treated kidney tissue. GAPDH served as an internal control. (d) qRT-PCR analysis was performed to detect the expression levels of proinflammatory cytokines in kidney tissue. The data are shown as the mean ± standard deviation (SD) of three independent experiments. (* P

    Article Snippet: For IHC, sections were incubated overnight at 4 °C with anti-HMGB1, anti-TLR4, anti-NF-kB, anti-SOD2 (Boster, China, BM4813) and anti-NOX2 (Boster, China, BA2811) antibodies and then detected using an Envision HRP Polymer System (Boster, China).

    Techniques: In Vivo, Light Microscopy, Staining, Immunohistochemistry, Expressing, Plasmid Preparation, Injection, Western Blot, Quantitative RT-PCR, Standard Deviation

    miR-216b reversed the effect of H19 on CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . (a) CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19-, miR-216b agonist-, or combination-treated CaOx nephrocalcinosis mouse models (magnification in all panels is 200 ×). Quantifications were performed using ImageJ. The data are shown as the mean ± SD of three independent experiments. (* P

    Journal: EBioMedicine

    Article Title: H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway

    doi: 10.1016/j.ebiom.2019.10.059

    Figure Lengend Snippet: miR-216b reversed the effect of H19 on CaOx nephrocalcinosis-induced renal tubular epithelial cell injury in vivo . (a) CaOx deposition in the corticomedullary junction area was measured by polarized light microscopy (Magnification, × 100) and Pizzolato staining (Magnification, × 200). PAS staining (Magnification, × 100) illustrating renal tubular epithelial cell injury. (b) Immunohistochemical analysis of kidney HMGB1, TLR4, NF-kB, SOD2 and NOX2 expression was performed in rAAV-H19-, miR-216b agonist-, or combination-treated CaOx nephrocalcinosis mouse models (magnification in all panels is 200 ×). Quantifications were performed using ImageJ. The data are shown as the mean ± SD of three independent experiments. (* P

    Article Snippet: For IHC, sections were incubated overnight at 4 °C with anti-HMGB1, anti-TLR4, anti-NF-kB, anti-SOD2 (Boster, China, BM4813) and anti-NOX2 (Boster, China, BA2811) antibodies and then detected using an Envision HRP Polymer System (Boster, China).

    Techniques: In Vivo, Light Microscopy, Staining, Immunohistochemistry, Expressing

    p38 activation leads to augmented oxidative stress in offspring of LPS-treated mothers after isoproterenol treatment and schematic illustration of the current study. Offspring were treated as described in Fig. 6 . ( a,b ) The mRNA levels of Nox2, Nox4, p67 phox , p47 phox , p22 phox ( a ) and Sod1, Sod2, Sod3 , catalase , Gpx1 ( b ) in left ventricle were determined by real-time RT-PCR. β-actin was taken as internal control. n = 5 offspring in each group. Error bar represents S.D. * p

    Journal: Scientific Reports

    Article Title: Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation

    doi: 10.1038/srep30146

    Figure Lengend Snippet: p38 activation leads to augmented oxidative stress in offspring of LPS-treated mothers after isoproterenol treatment and schematic illustration of the current study. Offspring were treated as described in Fig. 6 . ( a,b ) The mRNA levels of Nox2, Nox4, p67 phox , p47 phox , p22 phox ( a ) and Sod1, Sod2, Sod3 , catalase , Gpx1 ( b ) in left ventricle were determined by real-time RT-PCR. β-actin was taken as internal control. n = 5 offspring in each group. Error bar represents S.D. * p

    Article Snippet: The primary antibodies used were as followings: mouse anti-heavy chain cardiac Myosin (BA-G5) (α-MHC) (Abcam, Cambridge, MA, USA); mouse anti-skeletal slow myosin (NOQ7.5.4D) (β-MHC) (Sigma-Aldrich, St. Louis, MO, USA); rabbit anti-phospho- JNK(81E11), rabbit anti-JNK, rabbit anti-phospho-p38 MAPK (Thr180/Tyr182)(D3F9), rabbit anti-p38 MAPK, rabbit anti-phospho-ATF-2 (polyclone) (Cell signaling Technology, Beverly, MA, USA); rabbit anti-Nox2, rabbit anti-SOD1 and rabbit anti-SOD2 (Boster Wuhan, China).

    Techniques: Activation Assay, Quantitative RT-PCR

    Increased NADPH oxidase contributes to an imbalance of ROS generation and elimination in offspring from LPS-treated mothers after isoproterenol treatment. Offspring were treated as describe in Fig. 1 . ( a ) The mRNA levels and protein levels of ROS generation related genes (NADPH oxidase subunit, such as Nox2, Nox4, p67 phox , p47 phox and p22 phox ) in left ventricle were determined by real-time RT-PCR or immunoblotting, respectively. n = 5 offspring in each group. ( b ) The mRNA levels and protein levels of ROS elimination related genes (antioxidant enzymes, such as Sod1, Sod2, Sod3, catalase and Gpx1 ) in left ventricle were determined by real-time RT-PCR and immunoblotting, respectively. β-actin was taken as internal control in real-time RT-PCR. Representative plots in each group and statistical data of relative densitometry, normalized by GAPDH, are shown. n = 5 offspring in each group. Error bar represents S.D. * p

    Journal: Scientific Reports

    Article Title: Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation

    doi: 10.1038/srep30146

    Figure Lengend Snippet: Increased NADPH oxidase contributes to an imbalance of ROS generation and elimination in offspring from LPS-treated mothers after isoproterenol treatment. Offspring were treated as describe in Fig. 1 . ( a ) The mRNA levels and protein levels of ROS generation related genes (NADPH oxidase subunit, such as Nox2, Nox4, p67 phox , p47 phox and p22 phox ) in left ventricle were determined by real-time RT-PCR or immunoblotting, respectively. n = 5 offspring in each group. ( b ) The mRNA levels and protein levels of ROS elimination related genes (antioxidant enzymes, such as Sod1, Sod2, Sod3, catalase and Gpx1 ) in left ventricle were determined by real-time RT-PCR and immunoblotting, respectively. β-actin was taken as internal control in real-time RT-PCR. Representative plots in each group and statistical data of relative densitometry, normalized by GAPDH, are shown. n = 5 offspring in each group. Error bar represents S.D. * p

    Article Snippet: The primary antibodies used were as followings: mouse anti-heavy chain cardiac Myosin (BA-G5) (α-MHC) (Abcam, Cambridge, MA, USA); mouse anti-skeletal slow myosin (NOQ7.5.4D) (β-MHC) (Sigma-Aldrich, St. Louis, MO, USA); rabbit anti-phospho- JNK(81E11), rabbit anti-JNK, rabbit anti-phospho-p38 MAPK (Thr180/Tyr182)(D3F9), rabbit anti-p38 MAPK, rabbit anti-phospho-ATF-2 (polyclone) (Cell signaling Technology, Beverly, MA, USA); rabbit anti-Nox2, rabbit anti-SOD1 and rabbit anti-SOD2 (Boster Wuhan, China).

    Techniques: Quantitative RT-PCR