anti il 6 antibody  (Cell Signaling Technology Inc)


Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc anti il 6 antibody
    NaB alleviates inflammatory and fibrotic injury in DKD mice and high glucose-induced GMCs. Urine ACR (a), blood urea nitrogen (BUN) (b), blood crea (c), <t>serum</t> <t>IL-6</t> (d), and serum MCP-1 (e) were assayed at the 20th week of the experiment; H&E and Masson staining of mice in each group (×400) and immunohistochemistry were used to detect the expression of Fn in mouse kidney of each group (×400) (f). The expression of mainly the contents of collagen type IV (COL IV) in kidneys of each group was detected by immunofluorescence (×400) (g); qRT-PCR of Fn, TGF- β , IL-6, and MCP-1 in kidney tissue after NaB treatment (h, i); Western blotting-based assays for the expression of TGF- β and MCP-1 in GMCs after NaB intervention (j); GMCs were stimulated with 30 mM high glucose in the presence of the indicated concentration of NaB for 24 h. MCP-1 and IL-6 in the cell culture supernatant were evaluated by the kit (k, l). Values are presented as the mean ± SD. ∗ P < 0.05, ∗∗ 0.001 < P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.
    Anti Il 6 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti il 6 antibody/product/Cell Signaling Technology Inc
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti il 6 antibody - by Bioz Stars, 2023-11
    97/100 stars

    Images

    1) Product Images from "Sodium Butyrate Attenuates Diabetic Kidney Disease Partially via Histone Butyrylation Modification"

    Article Title: Sodium Butyrate Attenuates Diabetic Kidney Disease Partially via Histone Butyrylation Modification

    Journal: Mediators of Inflammation

    doi: 10.1155/2022/7643322

    NaB alleviates inflammatory and fibrotic injury in DKD mice and high glucose-induced GMCs. Urine ACR (a), blood urea nitrogen (BUN) (b), blood crea (c), serum IL-6 (d), and serum MCP-1 (e) were assayed at the 20th week of the experiment; H&E and Masson staining of mice in each group (×400) and immunohistochemistry were used to detect the expression of Fn in mouse kidney of each group (×400) (f). The expression of mainly the contents of collagen type IV (COL IV) in kidneys of each group was detected by immunofluorescence (×400) (g); qRT-PCR of Fn, TGF- β , IL-6, and MCP-1 in kidney tissue after NaB treatment (h, i); Western blotting-based assays for the expression of TGF- β and MCP-1 in GMCs after NaB intervention (j); GMCs were stimulated with 30 mM high glucose in the presence of the indicated concentration of NaB for 24 h. MCP-1 and IL-6 in the cell culture supernatant were evaluated by the kit (k, l). Values are presented as the mean ± SD. ∗ P < 0.05, ∗∗ 0.001 < P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.
    Figure Legend Snippet: NaB alleviates inflammatory and fibrotic injury in DKD mice and high glucose-induced GMCs. Urine ACR (a), blood urea nitrogen (BUN) (b), blood crea (c), serum IL-6 (d), and serum MCP-1 (e) were assayed at the 20th week of the experiment; H&E and Masson staining of mice in each group (×400) and immunohistochemistry were used to detect the expression of Fn in mouse kidney of each group (×400) (f). The expression of mainly the contents of collagen type IV (COL IV) in kidneys of each group was detected by immunofluorescence (×400) (g); qRT-PCR of Fn, TGF- β , IL-6, and MCP-1 in kidney tissue after NaB treatment (h, i); Western blotting-based assays for the expression of TGF- β and MCP-1 in GMCs after NaB intervention (j); GMCs were stimulated with 30 mM high glucose in the presence of the indicated concentration of NaB for 24 h. MCP-1 and IL-6 in the cell culture supernatant were evaluated by the kit (k, l). Values are presented as the mean ± SD. ∗ P < 0.05, ∗∗ 0.001 < P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Techniques Used: Staining, Immunohistochemistry, Expressing, Immunofluorescence, Quantitative RT-PCR, Western Blot, Concentration Assay, Cell Culture

    A485 inhibits NaB-mediated histone Kbu and reverses anti-inflammatory and antifibrotic effects. Effect of the P300 inhibitor A485 on the expression of PanKbu and H3K9bu by Western blotting (a). The expression of H3K9bu in the nucleus of GMCs in each group by Western blotting (b). The expression of PanKbu in GMCs of each group was detected by immunofluorescence (×200) (c). A485 had no significant effect on NaB-induced PanKac modification of GMCs (d). The NaB inhibition of TGF- β and MCP-1 was reversed by A485 (e). qRT-PCR was performed to detect Fn and TGF- β mRNA levels (f). The expression of IL-6 in cells of each group was detected by immunofluorescence (×200) (g). Values are presented as the mean ± SD. ∗ P < 0.05, ∗∗ 0.001 < P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.
    Figure Legend Snippet: A485 inhibits NaB-mediated histone Kbu and reverses anti-inflammatory and antifibrotic effects. Effect of the P300 inhibitor A485 on the expression of PanKbu and H3K9bu by Western blotting (a). The expression of H3K9bu in the nucleus of GMCs in each group by Western blotting (b). The expression of PanKbu in GMCs of each group was detected by immunofluorescence (×200) (c). A485 had no significant effect on NaB-induced PanKac modification of GMCs (d). The NaB inhibition of TGF- β and MCP-1 was reversed by A485 (e). qRT-PCR was performed to detect Fn and TGF- β mRNA levels (f). The expression of IL-6 in cells of each group was detected by immunofluorescence (×200) (g). Values are presented as the mean ± SD. ∗ P < 0.05, ∗∗ 0.001 < P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

    Techniques Used: Expressing, Western Blot, Immunofluorescence, Modification, Inhibition, Quantitative RT-PCR

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