Sustained pharmacological inhibition of δPKC protects against hypertensive encephalopathy through prevention of blood-brain barrier breakdown in rats
J. Clin. Invest. Xin Qi, et al. 118:173 doi:10.1172/JCI32636 [Go to this article.]

Figure 2
Sustained delivery of δV1-1 peptide inhibits hypertension-induced δPKC translocation. Rats fed a high-salt diet were treated with δV1-1, saline, or TAT as in Figure 1. Brain tissue was harvested at 13 weeks of age. (A) Soluble and particulate fractions of brain tissue were subjected to Western blot analysis, and δPKC translocation was determined. The blots show representative results, and the graph provides quantification of δPKC translocation from the cytosolic to the membranal fractions. Data are mean ± SEM (n = 3 rats per group). F = 13.68, df = 3. *P < 0.05 versus saline or TAT treatment; ^#P < 0.05 versus rats fed a low-salt diet (Nor). GAPDH and Gα were used as internal controls for cytosolic and membranal fractions, respectively. (B) Total lysates of the brain were subjected to Western blot analysis with anti-δPKC. GAPDH was used as an internal loading control. Representative data are from 3 rats per group. (C) Phosphorylation of δPKC (Ser643) was determined by Western blot analysis. Data are mean ± SEM (n = 3 rats per group). F = 11.49, df = 3. *P < 0.05 versus saline treatment groups; ^#P < 0.05 versus rats fed a low-salt diet.