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In this study, we investigated (1) the in vivo occurrence of CM-induced tubular renal cells apoptosis; (2) the in vitro and in vivo effects of CM on stress kinases and apoptotic pathways; (3) the in vitro effects CM on ROS production in renal tubular cells; and (4) the in vitro effects of stress kinases inhibition by different approaches in preventing the contrast-induced cell damage.
Cytoxic effects of CM on glomerular mesangial cells include apoptotic effects, associated with elevated intracellular ROS levels [37].
More effects of CM on tubular cells have been described, including redistribution of membrane proteins, reduction of extracellular Ca2+, DNA fragmentation, disruption of intercellular junctions, reduced cell proliferation, apoptosis and altered mitochondrial function [37].
However, the effects of CM on HCD-induced hepatic biochemical and structural changes, oxidative-antioxidative balance and glucose homeostasis have not been investigated.
This is the first study, to the best of our knowledge, to investigate the effects of CM on the biochemical and histological changes related to NAFLD.
To assess the molecular pathways leading to CM apoptosis activation, we determined the effects of CM on the formation of ROS.
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Figure 1D shows the effect of CM on sodium channel currents from 3 µM to 3 mM.
In light of this evidence, the effect of CM on the activation status of mTOR was assessed.
To clarify these conflicting findings, we investigated the effect of CM on the expression of cardiac progenitor markers.
A toxic effect of CM on renal tubules has been shown in both clinical trials and animal experiments.
CM-Post CM-Post Palmdepletedsofexosomeso effect on Akt level (Fig. 3d), indicating thad exosomes likely participated inotheffectct on CM on totAktAkt in C2C12 celevel
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