SCNN1A Antibody - #DF9199

Figure 2 Effects of renal lypla1 knockdown on blood pressure and sodium reabsorption in E. faecalis-treated mice (A) Expression of LYPLA1 in the renal medulla (n = 6 per group). (B) SBP and DBP (n = 6 per group). (C) Serum Ang II content (n = 6 per group). (D) Urinary sodium excretion (n = 6 per group). (E) Urine volume (n = 6 per group). (F) Representative immunoblots of αENaC and summarized intensities of blots in the renal medulla (n = 6 per group). Data are presented as mean ± SE. ∗p < 0.05, ∗∗p < 0.01; $ p < 0.05, $$ p < 0.01 VS other groups; ns, no significance. (G) Urinary sodium excretion (n = 6 per group). (H) Representative immunoblots of αENaC and summarized intensities of blots in the renal medulla (n = 6 per group). Data are presented as mean ± SE. ∗p < 0.05, ∗∗p < 0.01; $ p < 0.05, $$ p < 0.01 VS other groups; ns, no significance.

Fig. 11. Exposed protein bands (A) and grayscale ratios of VIP (B1), CAP1 (B2), PKA (B3), CFTR (B4), NHE3 (B5), ENaC (B6), AQP3 (B7), AQP4 (B8), and AQP8 (B9) protein expression in the colon of each group. # P < 0.05, ## P < 0.01 vs. Nor group; * P < 0.05, * * P < 0.01 vs. Mod group.

Figure 4.| Treatment with SWNHs alters the expression of mitochondrial apoptosis pathway-associated proteins in vivo. HepG2 xenografts in nude mice were regularly treated with SWNHs. The changes in expression and relative quantification of mitochondrial apoptosis pathway-associated proteins that were induced by SWNHs as detected by western blotting in HepG2 xenografts. Data are presented as the mean ± standard deviation (n=3). P<0.05 compared with the control group. AceCS2, acyl-CoA synthetase short chain family member 1; SCNN1A, sodium channel epithelial 1α subunit; SIRT3, sirtuin 3; SWNH, single-walled carbon nanohorn; VDAC1, voltage‑dependent anion channel 1

Fig. 4 |Effects of NaBu on DOCA/salt-induced renal sodium transporter proteins.Representative immunoblots of α-ENaC, β-ENaC, γ-ENaC,NHE3, NCC, and NKCC-2 and summarized intensities of blots in the renal cortex (a) and medulla (b) (n = 6–7 per group).αENaC α-subunit of epithelial sodium channel, β-ENaC βsubunit of epithelial sodium channel, γ-ENaC γ-subunit of epithelial sodium channel,NHE3 sodium/proton exchanger isoform 3, NKCC-2 Na-K-2Cl cotransporter, NCC Na-Cl Cotransporter

Fig. 6. Effects of Cacna1d D307G mutation on sodium homeostasis and protein expression of ETA and ET-1 in the renal artery; protein expression of ETA and ETB in the renal cortex; protein expression of ETB in the renal medulla; and protein expression of αENaC in the kidney. a Plasma sodium level in the three different genotype groups fed with NSD and HSD. b Urinary sodium excretion in the three different genotype groups fed with NSD and HSD. c Western blot analysis of ETA and ET-1 in the renal artery; GAPDH was used as the internal control. d Western blot analysis of ETA and ETB in the renal cortex; GAPDH was used as the internal control. e Western blot analysis of ETB in the renal medulla; GAPDH was used as the internal control. f, g Western blot analysis of αENaC in the renal cortex and the medulla; β-actin was used as the internal control. All data are presented as mean ± SD, n = 6; ns, p > 0.05, *p < 0.05, **p < 0.01 vs. WT+HSD. SD, standard deviation.