Polydatin Protecting Kidneys against Hemorrhagic Shock-Induced Mitochondrial Dysfunction via SIRT1 Activation and p53 Deacetylation

Figure 3

Effect of polydatin (PD) administration on mitochondrial apoptosis pathway-related protein expression and renal function after hemorrhagic shock. (a, b) TUNEL staining of renal cortex (original magnification, ×400); (c) western blotting of expression of PUMA-α, Bcl-2, Bax, cytoplasm cytochrome C (cyto-cytC), and mitochondrial cytochrome C (mito-cytC), and cleaved caspase-3; (d) quantitation of PUMA-α, (e) Bax, (f) Bcl-2, and (h) cleaved caspase-3 protein, ; (g) cytoplasm/mitochondria (cyto/mito) ratio of cytochrome C ( in each group); (i) immunohistochemistry of the proapoptotic protein Bax and antiapoptotic protein Bcl-2; (j) determination of levels of blood urea nitrogen and (k) creatinine, . , compared with the value of the vehicle group; , compared with the value of the vehicle group; , compared with the value of the PD group. DAPI, 4′,6-diamidino-2-phenylindole; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; FITC, fluorescein isothiocyanate; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling.

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