Abstract
We investigated whether 14 phenolic compounds isolated from Artemisia argyi could prevent the apoptotic damage caused by iodixanol, an iodinated contrast agent, on LLC-PK1 cells. Iodixanol was used to induce cytotoxicity in LLC-PK1 cells. Apoptotic cell death was observed as the fluorescence intensity emitted by annexin V and Hoechst 33342 stains. Western blotting was used to detect specific proteins. Seven phenolic compounds protected against iodixanol-induced LLC-PK1 cell death in a concentration-dependent manner. Among them, methyl caffeate exerted the strongest protective effect, and co-treatment with 50 and 100 μM methyl caffeate decreased intracellular reactive oxygen species elevated by 25 mg/mL iodixanol. In addition, the treatment of LLC-PK1 cells with iodixanol resulted in an increase in apoptotic cell death, which decreased by co-treatment with methyl caffeate. Iodixanol caused a cytotoxicity-related increase in the phosphorylation of extracellular-signal-regulated kinase, c-Jun N-terminal kinase, and P38; and a similar increase in the expression levels of kidney injury molecule-1 and cleaved caspase-3. However, the up-regulation of these proteins was reversed by co-treatment with methyl caffeate. These findings suggest that phenolic compounds isolated from A. argyi play an important role in protecting kidney epithelium cells against apoptotic damage caused by iodixanol.
Highlights
Contrast agents are widely used to improve the visibility of blood vessels and internal organs, including the tissues and urinary tract in patients undergoing elective coronary procedures [1].Based on osmolality, contrast agents are classified into three distinct groups—nonionic low-osmolar iopromide, ionic ioxitalamate, and isoosmolar iodixanol [1,2]
We showed that artemetin, a flavonoid isolated from A. argyi, can protect against contrast agent-induced cytotoxicity in renal proximal tubular cells through the inhibition of reactive oxygen species (ROS) generation and apoptosis [28]
Protective Effect of Phenolic Compounds Isolated from A. argyi on Iodixanol-Induced Renal Proximal
Summary
Contrast agents are widely used to improve the visibility of blood vessels and internal organs, including the tissues and urinary tract in patients undergoing elective coronary procedures [1].Based on osmolality, contrast agents are classified into three distinct groups—nonionic low-osmolar iopromide, ionic ioxitalamate, and isoosmolar iodixanol [1,2]. The major reasons for cytotoxicity are the reduction in medullary blood flow and direct renal proximal tubular cell damage. The latter is related to the hypoxia-mediated formation of reactive oxygen species (ROS) [2,8,9]. The prevention of the formation of ROS can be beneficial in protecting against contrast agent-induced renal proximal tubular cell damage. Many studies have demonstrated that N-acetylcysteine (NAC), a known antioxidant, prevents contrast agent-induced nephrotoxicity in the human embryonic kidney cell line, the porcine renal proximal tubular cell line, and the canine Madin-Darby distal tubular renal cell line [1,8,10]. Vitamin E protects against contrast agent-induced nephrotoxicity in patients undergoing elective coronary procedures [11,12]
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