Abstract
Calorie restriction (CR) extends lifespan and increases resistance to multiple forms of stress, including renal ischemia-reperfusion (I/R) injury. However, whether CR has protective effects on contrast-induced nephropathy (CIN) remains to be determined. In this study, we evaluated the therapeutic effects of CR on CIN and investigated the potential mechanisms. CIN was induced by the intravenous injection of iodinated contrast medium (CM) iopromide (1.8 g/kg) into Sprague Dawley rats with normal food intake or 40% reduced food intake, 4 weeks prior to iopromide administration. We found that CR was protective of CIN, assessed by renal structure and function. CM increased apoptosis, reactive oxygen species (ROS), and inflammation in the renal outer medulla, which were decreased by CR. The silent information regulator 1 (SIRT1) participated in the protective effect of CR on CIN, by upregulating glutathione peroxidase 4 (GPX4), a regulator of ferroptosis, because this protective effect was reversed by EX527, a specific SIRT1 antagonist. Our study showed that CR protected CIN via SIRT1/GPX4 activation. CR may be used to mitigate CIN.
Highlights
Contrast-induced nephropathy (CIN) is the abrupt deterioration of renal function resulting from intravenous or intra-arterial administration of iodinated contrast media used in diagnostic coronary angiography or percutaneous coronary intervention [1, 2]
Our study showed that silent information regulator 1 (SIRT1) expression, determined by immunoblotting, was lower in the contrast medium (CM) group, compared with that control group, which was reversed by Calorie restriction (CR) (Figure 3(a))
The degree of apoptosis, oxidative stress, and inflammation was attenuated in the CR-treated CM group, relative to the CM group on normal caloric intake, which further confirmed the protective effect of CR in CIN
Summary
Contrast-induced nephropathy (CIN) is the abrupt deterioration of renal function resulting from intravenous or intra-arterial administration of iodinated contrast media used in diagnostic coronary angiography or percutaneous coronary intervention [1, 2]. The frequency of CIN ranges from 2% in low-risk patients to 50% in high-risk patients. It is reported to be the third leading cause of hospitalacquired acute renal injury. CIN is associated with increased morbidity, extended length of hospital stays, and increased costs [3,4,5]. The precise mechanism underlying CIN is not fully understood. A decrease in renal blood flow, increased reactive oxygen species (ROS) formation, and direct toxic affection renal tubule cells may be involved in the pathogenesis of CIN [6, 7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
