Fig. 6.

Treatment of LDN suppresses Ang II-induced oxidative stress, inflammation and downstream mediators in mice. a Immunoblotting analyses of the profibrotic signaling molecules p-AKT, AKT, p-ERK1/2, ERK1/2, and tubulin in the heart. The quantification of the relative protein levels (n = 4). b Immunoblotting analyses of fibrosis, oxidative stress and the inflammatory mediators HIF-1α, TGF-β1, p-Smad2/3, Smad2, Smad3, and CX43 in the heart. The quantification of the relative protein levels (n = 4). α-Tubulin was used as an internal control. n represents the number of animals (n = 4). ^*P < 0.05, ^**P < 0.01 versus saline control; ^#P < 0.05 versus Ang II alone. c A working model of the effect of LDN administration on Ang II-induced AF. Treatment with LDN suppresses Ang II-induced oxidative stress and inflammatory mediators (AKT, ERK1/2, HIF-1α, and TGF-β/Smad2/3) in mice