Contrast Media-Induced Nephropathy in Patients with Unruptured Cerebral Aneurysm After Coiling Endovascular Treatment

Joo, Chunghee; Park, Eunhye; Min, Joo-Won; Kang, Hyun; Yoo, Do Sung; Jung, Hyun Ju

doi:10.1016/j.wneu.2018.08.206

Cited by 4 publications

(1 citation statement)

References 24 publications

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“…In patients undergoing coronary angiography or percutaneous coronary intervention, the incidence of CIN is as high as 20% to 25% (1). CIN is usually defined as an absolute increase of 0.5 mg/dL or a relative increase of 25% in serum creatinine within 48-72 hours after contrast exposure (2). But it is recommended that CIN should be also considered in the presence of acute renal failure within 7 days of exposure (3).…”

Section: Introductionmentioning

confidence: 99%

Inhibiting PKCβ2 protects HK-2 cells against meglumine diatrizoate and AGEs-induced apoptosis and autophagy

Jiang¹,

Zhao²,

Ye³

et al. 2020

Ann Transl Med

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Background: Contrast induced diabetic nephropathy (CIN) is an important cause of hospital-acquired acute renal failure. Our aim was to observe the effect of protein kinase C β2 (PKCβ2) knockdown on human proximal tubular epithelial cells (HK-2 cells) against meglumine diatrizoate and advanced glycation end products (AGEs)-induced apoptosis and autophagy.Methods: Cell viability was detected using cell counting kit-8 (CCK-8) assay in HK-2 cells after disposal with meglumine diatrizoate and AGEs with or without PKCβ2 siRNA/inhibitor LY333531. Flow cytometry and western blot were used to test cell apoptosis and the related protein levels in meglumine diatrizoate and AGEs co-treated HK-2 cells with or without PKCβ2 siRNA/inhibitor LY333531. Autophagy related proteins were detected using western blot. Immunofluorescence staining was used to examine the autophagyspecific protein light chain 3 (LC3), and autophagosome and autolysosome formation was observed under a transmission electron microscopy.Results: CCK-8 assay results showed that meglumine diatrizoate inhibited AGEs-induced HK-2 cell viability. Furthermore, meglumine diatrizoate promoted cell apoptosis and the expression level of caspase3 in AGEs-induced HK-2. Western blot results showed that meglumine diatrizoate elevated the expression levels of PKCβ2 and p-PKCβ2 in AGEs-induced HK-2 cells, and up-regulated the expression level of Beclin-1 and the ratio of LC3 II/LC3 I, and down-regulated the expression level of p62 in AGEs-induced HK-2 cells. We found that PKCβ2 knockdown alleviated meglumine diatrizoate and AGEs-induced HK-2 cell apoptosis and autophagy. Intriguingly, PKCβ2 inhibitor LY333531 reversed 3-methyladenine (3-MA)-induced autophagy inhibition in meglumine diatrizoate and AGEs-induced HK-2 cells.Conclusions: Our findings reveal that inhibiting PKCβ2 protects HK-2 cells against meglumine diatrizoate and AGEs-induced apoptosis and autophagy, which provide a novel therapeutic insight for CIN in diabetic patients.

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Section: Introductionmentioning

confidence: 99%