Naringenin Ameliorated Kidney Injury through Let-7a/TGFBR1 Signaling in Diabetic Nephropathy

Figure 5

NAR inhibited TGF-β1/smads signaling through let-7a in vivo and in vitro. (a) Real-time RT PCR showed the mRNA levels of TGF-β1, TGFBR1, smad2, and smad7 of kidney tissues in rats. (b) Western blot analysis of TGF-β1, TGFBR1, smad2, p-smad2, and smad7 proteins in kidney tissues and MMCs. (c) Quantifications of the western blot bands of TGF-β1, TGFBR1, smad7, and p-smad2 expressions in DN rats. (d) Quantifications of the western blot bands of TGF-β1, TGFBR1, smad7, and p-smad2 expressions in MMCs. (e) Immunofluorescence of TGF-β1 and TGFBR1 proteins in kidney tissues of rats. (f) Western blot analysis of TGFBR1, smad2, and p-smad2 proteins in MMCs transferring let-7a mimics or inhibitor with NAR. (g) Quantifications of the western blot bands of TGFBR1 and p-smad2 expressions in MMCs transferring let-7a mimics or inhibitor with NAR. (a) Results were normalized with GAPDH and expressed as mean ± standard deviation ( per group). ; versus CON group; ; versus DN group. (c) Results were normalized with GAPDH and expressed as mean ± standard deviation ( per group). versus CON group; ; versus DN group. (d) Results were normalized with GAPDH and expressed as mean ± standard deviation ( per group). ; versus LG group; ; versus HG group. (g) Results were normalized with GAPDH and expressed as mean ± standard deviation ( per group). ; versus LG group; ; versus HG group.

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