Research Paper Volume 11, Issue 11 pp 3716—3730
Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis
Figure 8. MEG3 overexpression enhanced DN development in vivo. (A) Establishment procedure of overexpressed MEG3 in DN rat models (LV-MEG3 group = 12, LV-NC group = 12). (B) QPCR results showed that MEG3 was successfully overexpressed in DN tissues after LV-MEG3 injection. (C) HE staining results as demonstrated in the microscope. (D) MEG3 overexpression increased the urinary albumin excretion rate in DN rat models. (E) QPCR results showed that miR-181a expression was downregulated in DN after LV-MEG3 injection. (F, G) MEG3 overexpression increased the mRNA expression of Egr-1 and TLR4. (H) MEG3 overexpression increased the protein expression of Egr-1 and TLR4 in vivo. (I–K) MEG3 overexpression increased the mRNA expression of TGFβ1 (H), TNF-α (I), and α-SMA (J) in vivo. (L) Western blot results indicated that MEG3 overexpression increased the protein expression of TGFβ1, TNF-α, and α-SMA.