ArticleClinical and experimental nephrology2009
Serofendic acid protects from iodinated contrast medium and high glucose probably against superoxide production in LLC-PK1 cells.
Article in Clinical and experimental nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 12 citations in OpenAlex.
- Assessment of an advanced virtual monoenergetic reconstruction technique in cerebral and cervical angiography with third-generation dual-source CT: Feasibility of using low-concentration contrast medium.European radiology · 2018Trial
- The Ameliorative Role ofAntioxidants (Basel, Switzerland) · 2021Article
- Albumin and glycated albumin activate KIM-1 release in tubular epithelial cells through distinct kinetics and mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Hu-Lu-Ba-Wan Attenuates Diabetic Nephropathy in Type 2 Diabetic Rats through PKC- α /NADPH Oxidase Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
backgroundIt is well known that patients with chronic kidney disease, including diabetic nephropathy, often develop cardiovascular diseases. In case of radiographic procedures, reduced renal function may be deteriorated by the use of iodinated contrast medium (CM). This is known as CM-induced nephropathy. In this study, we have focused on the mechanisms of this type of injury in diabetic nephropathy and the preventive effects of serofendic acid.
methodsWe evaluated the cytotoxicity of CM and high glucose on tubular epithelial cells using an LLC-PK1 cell line, and measured cell viability with an alamarBlue assay. We further evaluated superoxide production levels measured by dihydroethidium. We also examined the protective effects of serofendic acid on cytotoxicity with superoxide production of CM and high glucose.
resultsCM reduced cell numbers in a dose-dependent and time-dependent manner in LLC-PK1 cells. Furthermore, cytotoxicity of CM in diluted concentration was additively influenced by high glucose. CM and high glucose increased superoxide production, which was evaluated by the response to dihydroethidium, and was suppressed by serofendic acid. Cytotoxicity of CM, high glucose, and H(2)O(2) was suppressed by serofendic acid, as well as the suppression by N-acetylcysteine on CM toxicity. Interestingly, the recovery by serofendic acid in H(2)O(2)- and high glucose-induced cellular injury was to the basal level, in contrast with the partial recovery from CM-induced injury. Finally, serofendic acid suppressed CM-induced injury and high glucose-induced apoptosis.
conclusionsThese results suggest that CM and high glucose induce cytotoxicity and oxidative stress in LLC-PK1 cells and that serofendic acid protects the injury probably from superoxide generation.
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