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

Figure 5

Effect of polydatin (PD) administration on the morphology and function of mitochondria in RTECs after HS/R and in HK-2 cells after H/R, respectively. (a) Ultrastructural alterations in RTEC mitochondria were detected using TEM (original magnification, ×11,500); (b) quantification of RTEC mitochondrial depolarization expressed as changes in the JC-1 fluorescence monomer/aggregate ratio (–6); (c) intracellular level of ATP in RTECs (). (d–f) mPTP in RTECs was observed using confocal microscopy (original magnification, ×630) and quantified using flow cytometry (); (g–i) mPTP (reflected by the fluorescence intensity of calcein-AM) in HK-2 cells was observed using a microscope (original magnification, ×630) and quantified using flow cytometry; (j) quantification of depolarization of mitochondria in HK-2 cells as JC-1 monomer/aggregate using flow cytometry; (k) intracellular level of ATP in HK-2 cells using a luciferase-based assay ( in each group). , compared with the value of the vehicle group; , compared with the value of the vehicle group; , compared with the value of the PD group; compared with the value of the PD/Ex527 group. HK-2, human kidney-2; H/R, hypoxia/reoxygenation; HS/R, hemorrhagic shock and reperfusion; mPTP, mitochondrial permeability transition pore; RTECs, renal tubular epithelial cells; TEM, transmission electron microscopy.

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