Vitamin E (α-tocopherol) ameliorates aristolochic acid-induced renal tubular epithelial cell death by attenuating oxidative stress and caspase-3 activation
| Autor: | Ying‑Ru Pan, Hsueh Fang Wang, Chyou Wei Wei, Tsai Kun Wu, Yung Luen Yu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Antioxidant Cell Survival medicine.medical_treatment caspase aristolochic acid alpha-Tocopherol Aristolochic acid Caspase 3 Apoptosis vitamin E Pharmacology medicine.disease_cause Biochemistry Cell Line 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine renal tubular epithelial cells Genetics medicine Animals Molecular Biology Caspase chemistry.chemical_classification Reactive oxygen species α-tocopherol biology Dose-Response Relationship Drug Vitamin E Epithelial Cells Articles Hydrogen Peroxide Rats Oxidative Stress 030104 developmental biology Kidney Tubules Oncology chemistry 030220 oncology & carcinogenesis biology.protein Cancer research Molecular Medicine Aristolochic Acids Reactive Oxygen Species Oxidative stress |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | Aristolochic acid (AA) is a component identified in traditional Chinese remedies for the treatment of arthritic pain, coughs and gastrointestinal symptoms. However, previous studies have indicated that AA can induce oxidative stress in renal cells leading to nephropathy. α‑tocopherol exists in numerous types of food, such as nuts, and belongs to the vitamin E isoform family. It possesses antioxidant activities and has been used previously for clinical applications. Therefore, the aim of the present study was to determine whether α‑tocopherol could reduce AA‑induced oxidative stress and renal cell cytotoxicity, determined by cell survival rate, reactive oxygen species detection and apoptotic features. The results indicated that AA markedly induced H2O2 levels and caspase‑3 activity in renal tubular epithelial cells. Notably, the presence of α‑tocopherol inhibited AA‑induced H2O2 and caspase‑3 activity. The present study demonstrated that antioxidant mechanisms of α‑tocopherol may be involved in the increased survival rates from AA‑induced cell injury. |
| Databáze: | OpenAIRE |
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