Abstract
Patients with chronic kidney disease (CKD) are at an increased risk of premature death due to the development of cardiovascular disease (CVD) owing to atherosclerosis-mediated cardiovascular events. However, the mechanisms linking CKD and CVD are clear, and the current treatments for high-risk groups are limited. In this study, we aimed to examine the effects of sesamol, a natural compound extracted from sesame oil, on the development of atherosclerosis in a rodent CKD model, and reactive oxygen species-induced oxidative damage in an endothelial cell model. ApoE–/– mice were subjected to 5/6 nephrectomy (5/6 Nx) and administered sesamol for 8 weeks. Compared with the sham group, the 5/6 Nx ApoE–/– mice showed a significant increase in malondialdehyde levels and Oil Red O staining patterns, which significantly decreased following sesamol administration. Sesamol suppressed H2O2-induced expression of phospho-IKKα, p53, and caspase-3. Our results highlight the protective role of sesamol in renal injury-associated atherosclerosis and the pathological importance of oxidative stress burden in CKD–CVD interaction.
Highlights
Patients with chronic renal failure are at an increased risk of premature mortality, which is associated with an increased incidence of atherosclerotic cardiovascular complications [1]
To investigate the effect of SM on oxidative stress, we evaluated the effect of SM supplementation on lipid peroxidation by measuring the MDA level in the kidney, plasma, and carotid artery
To investigate whether SM is an effective therapeutic agent for Chronic kidney disease (CKD)-mediated atherosclerosis, we assessed the effect of SM on atherosclerotic lesions in 5/6 Nx ApoE–/
Summary
Patients with chronic renal failure are at an increased risk of premature mortality, which is associated with an increased incidence of atherosclerotic cardiovascular complications [1]. Atherosclerosis and cardiovascular diseases (CVDs) occur due to the imbalances between the production and scavenging of free radicals during physiological processes, thereby leading to inflammation, apoptosis, and lipid, protein, or nucleic acid damage [2]. Chronic kidney disease (CKD) is associated with high levels of ROS generation [3]. Hydrogen peroxide (H2 O2 ) is a major ROS generated during ischemia–reperfusion injury and is produced in animal models of chronic brain disease [4]. Endothelial cells have a fundamental role in various pathological and physiological processes. They can synthesize and release catecholamines in response to ischemia, highlighting their importance in controlling vascular homeostasis [7].
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