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 5. Inhibition of miR-181a upregulated the expression of fibrosis-related proteins and concentration of inflammatory cytokines. (A) The efficiency of miR-181a inhibitor was determined by qPCR. (B-D) MiR-181a inhibition increased the mRNA expression level of TNF-α (B), α-SMA (C), and TGF-β1 (D) in MCs based on ELISA. (E) MiR-181a inhibition increased the protein expression level of TNF-α, α-SMA, and TGF-β1 in MCs. (F-I) MiR-181a inhibition increased the concentrations of CRP (F), IL-1β (G), IL-6 (H), and MCP-1 (I) in MCs based on ELISA.