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논문 기본 정보

자료유형
학술저널
저자정보
Promise M.Emeka (Department of Pharmaceutical Sciences College of Clinical Pharmacy King Faisal University Al-Ahsa 3) Sahibzada T. Rasool (Department of Biomedical Sciences College of Clinical Pharmacy King Faisal University Al-Ahsa 31982) Mohamed A.Morsy (Department of Pharmaceutical Sciences College of Clinical Pharmacy King Faisal University Al-Ahsa 3) Mohamed I. Islam Hairul (Department of Biological Sciences College of Science King Faisal University Al-Ahsa 31982 Saudi Ara) Muhammad S.Chohan (Department of Biomedical Sciences College of Clinical Pharmacy King Faisal University Al-Ahsa 31982)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제25권 제4호
발행연도
2021.1
수록면
321 - 331 (11page)

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Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin- induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPAR?) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl- ?-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPAR?, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-?B) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-?B expression increased. Lutein ameliorated these effects, and significantly increased PPAR? expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPAR?/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-?B and apoptosis by caspase-3.

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