Fig. 7.

SRT1720 normalises inflammatory and reparative cell damage in the bone marrow and blood of db/db mice with 6 month duration of diabetes. (a, b) Tnf-α (n=4–5 mice) (a) and Ccl-2 (n=5 mice carried out in duplicate) (b) expression in the bone marrow of non-diabetic controls, and diabetic mice fed normal chow or chow containing SRT1720. (c, d) Diabetes significantly decreases the number of MEPs (c) and CACs (d) in the bone marrow, while SRT1720 restores MEP to non-diabetic levels, n=4–5. (e, f) In the blood, diabetes significantly decreases the number of reparative CACs (e) and increases the number of inflammatory circulating total monocytes (f); n=4–5. (g, h) In M2 macrophages, diabetes induces decrease in the expression of Lxrα and LXR-controlled target genes (Abca1 and Abcg1). SRT1720 increases Sirt1 expression in M2 macrophages (g), leading to upregulation of LXR activity as shown by an increase in Abcg1 expression (h); n=4–5; *p<0.05, **p<0.01, ***p<0.001. Data are represented as mean ± SEM. Ctl, control (db/m); CycloA, cyclophilin A; D, diabetic (db/db); LS-K, Lin⁻Sca⁻Kit⁺