Journal: Biochemical pharmacology
Article Title: Butyrate promotes kidney resilience through a coordinated kidney protective response in tubular cells.
doi: 10.1016/j.bcp.2024.116203
Figure Lengend Snippet: Fig. 13. Conceptual representation of the impact of butyrate increasing kidney resilience by preserving kidney protective genes. A) Either the initial insult or inflammation promotes the activation of NFκB and histone deacetylation in tubular cells. As a result, genes encoding inflammatory mediators are transcribed, potentially amplifying inflammation and injury, while genes encoding kidney protective genes are suppressed. Through inhibition of NFκB activation and histone deacetylation, butyrate decreases inflammation and preserves the expression of kidney protective genes. B) To assess the relative contribution of the preservation of kidney protective genes, mice were administered recombinant Klotho, which reproduced the effect of butyrate increasing kidney resilience by preserving the expression of other kidney protective genes and decreasing kidney inflammation.
Article Snippet: In a second cisplatin-AKI model, C57BL/6 mice were dosed intraperitoneally with recombinant mouse Klotho (rKlotho; 10 μg/kg, intraperitoneal injection; R&D System, Minneapolis, MN) or vehicle once a day starting one day before the cisplatin injection.
Techniques: Preserving, Activation Assay, Inhibition, Expressing, Recombinant