Figure 6. GSK3β overactivity and NFkB activation in glomeruli in LPS-injured mice were mitigated after valproate therapy, resulting in a blunted podocyte acquisition of immune phenotypes and podocytopathy.

Mice were treated as stated in Figure 5 and mouse kidneys were procured for further examination. A. and C. Isolated glomeruli were processed for immunoblot analysis for diverse molecules. B. and D. Immunoblots were subjected to densitometric analysis and arbitrary units were expressed respectively as immunoblot densitometric ratios of diverse molecules to actin as folds of the control group. *P < 0.05 versus the level of the same molecule in LPS-injured mice without VPA treatment (n = 6). E. Frozen sections of mouse kidneys were processed for dual color fluorescent immunohistochemistry staining for indicated immune molecules and podocyte marker proteins. Representative microscopic images were shown. Bar = 50 µm. CTSL, cathepsin L; LPS, lipopolysaccharide; SYNPO, synaptopodin; VPA, sodium valproate.