Research Paper Volume 11, Issue 20 pp 8745—8759

Long noncoding RNA GAS5 inhibits cell proliferation and fibrosis in diabetic nephropathy by sponging miR-221 and modulating SIRT1 expression

Figure 8. Upregulation of lncRNA GAS5 alleviated DN in vivo. (A) H&E staining of DN results. The LV-GAS5 group was injected with LV-GAS5, and the LV-NC group was injected with LV-NC (LV-GAS5 group=8, LV-NC group=8); (B) The expression level of lncRNA GAS5 was measured by qPCR in both groups; (C) Urinary albumin excretion rate was decreased in the LV-GAS5 group compared with that in the LV-NC group; (DF) The expression level of FN (D), Col-4 (E), and TGFβ1 (F) were measured by qPCR in the DN rat model transfected with LV-GAS5 or LV-NC; (GH) The expression level of FN, Col-4, and TGFβ1 were measured by western blot in the DN rat model transfected with LV-GAS5 or LV-NC; (I) qPCR results revealed that the expression level of miR-221 decreased in the DN rat model transfected with LV-GAS5; (JL) The expression level of SIRT1 was upregulated in the DN rat model transfected with LV-GAS5; (MO) The expression level of p53 was upregulated in DN transfected with LV-GAS5; (P) qPCR results revealed that there is positively correlation between lncRNA GAS5 and SIRT1 (Figure 8P). (Q) The relationship between the expression level of GAS5 and SIRT1 was detected by qPCR in T2D with DN tissues (N=30). *P < 0.05, **P < 0.01.