Effect of trans-sodium crocetinate on contrast-induced cytotoxicity in HEK-۲۹۳ cells

Publish Year: 1402
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:

JR_IJBMS-26-2_003

تاریخ نمایه سازی: 8 دی 1401

Abstract:

Objective(s): Contrast media (CM) are used for diagnostic or therapeutic intervention purposes in medicine. The main adverse reaction after the administration of CM is contrast-induced nephropathy (CIN). This complication is the third cause of renal failure after hospital treatment. The current study is designed to investigate the possible protective effect of trans-sodium crocetinate (TSC), derived from carotenoid crocetin, against sodium amidotrizoate/meglumine amidotrizoate (SAMA) induced cytotoxicity in HEK-۲۹۳ cells.Materials and Methods: HEK-۲۹۳ cells were incubated with different concentrations of TSC (۱, ۲.۵, ۵, ۱۰, ۲۵, and ۵۰ µM, for ۴۸ hr) and then SAMA (۷ mgI/ml, for ۲۴ hr) was added. The cell viability, intracellular ROS, and phosphatidyl serine exposure were detected by MTT assay, DCFH-DA, and annexin V-FITC/PI method, respectively. The P-ERK/ERK ratio, apoptosis (Bax/Bcl-۲ ratio and cleaved caspase-۳), and autophagy (LC۳ II/I ratio and beclin-۱) markers in cells were evaluated by the western blot method.Results: The exposure of HEK-۲۹۳ cells to SAMA reduced viability, increased apoptotic cells, enhanced ROS production, and subsequently decreased P-ERK/ERK ratio. Similarly, SAMA enhanced apoptosis (Bax/Bcl-۲ ratio and cleaved caspase-۳) and autophagy (LC۳ II/I ratio and beclin-۱) markers in HEK-۲۹۳ cells. The pretreatment of cells with TSC before exposure to SAMA significantly attenuated contrast-induced cytotoxicity. TSC reduced intracellular ROS production and activated the phosphorylation of ERK. In addition, TSC decreased the levels of apoptosis and autophagy proteins. Conclusion: The pretreatment of HEK-۲۹۳ cells with TSC can decrease contrast-induced cytotoxicity through antioxidant effect and modulate  ERK, apoptosis, and autophagy pathways.

Authors

Fatemeh Rajabian

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Soghra Mehri

Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

BiBi Marjan Razavi

Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Abolfazl Khajavirad

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Mahboobeh Ghasemzadeh Rahbardar

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Hossein Hosseinzadeh

Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

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