Both ERK/MAPK and TGF-Beta/Smad Signaling Pathways Play a Role in the Kidney Fibrosis of Diabetic Mice Accelerated by Blood Glucose Fluctuation

<table>BGF treatment upregulated TGF-<i>β</i>1 expression and activated TGF-<i>β</i>1-induced smad signaling. (a) TGF-<i>β</i>1 expression in the kidney of mice was evaluated by RT-PCR. (b) Data are expressed as the mean ± SEM of three separate experiments.  <svg height="13.95" id="M11" style="vertical-align:-0.1638pt" version="1.1" viewbox="0 0 66.324997 13.95" width="66.324997" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink">
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</svg>  as compared to the control. (c) The phosphorylated forms of smad2 and smad3 were analyzed by Western blot, using either rabbit anti-p-smad2 or rabbit anti-p-smad3 and total rabbit anti-smad2/3 antibody.</table>

Journal of Diabetes Research

fig5

Figure 5

Figure 5: Both ERK/MAPK and TGF-Beta/Smad Signaling Pathways Play a Role in the Kidney Fibrosis of Diabetic Mice Accelerated by Blood Glucose Fluctuation 

Figure 5 | Both ERK/MAPK and TGF-Beta/Smad Signaling Pathways Play a Role in the Kidney Fibrosis of Diabetic Mice Accelerated by Blood Glucose Fluctuation 