Sodium Butyrate Attenuates Diabetic Kidney Disease Partially via Histone Butyrylation Modification

Figure 2

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 . .

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