Tetrahydrocurcumin Ameliorates Tacrolimus-Induced Nephrotoxicity Via Inhibiting Apoptosis |
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| Institution: | 1. Department of Surgery, Ulsan University, College of Medicine, Gangneung Asan Hospital, Gangneung, South Korea;2. College of Korean Medicine, Gachon University, Seongnam, South Korea;1. Department of Surgery, Nippon Medical School Chiba Hokusou Hospital, Chiba, Japan;2. Department of Transplant Surgery, Jichi Medical University, Tochigi, Japan;3. Department of Surgery, Nippon Medical School, Tokyo, Japan;1. Division of Nephrology, Department of Internal Medicine, Lin Shin Hospital, Taichung, Taiwan;2. Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan;3. Institute of Medicine, Chung-Shan Medical University, Taichung, Taiwan;4. School of Medicine, China Medical University, Taichung, Taiwan;1. Department of General, Vascular and Transplant Surgery, Medical University of Silesia, Katowice, Poland;2. Department of Histology and Embryology, Medical University of Silesia, Katowice, Poland;3. Department of Applied Pharmacy and Drug Technology, Sosnowiec, Poland;4. Biochefa Pharmaceutical Research Production Plant, Sosnowiec, Poland |
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| Abstract: | BackgroundCalcineurin inhibitors are effective immunosuppressive agents, but associated adverse effects such as nephrotoxicity may limit efficacy. Tacrolimus (FK506) is an immunosuppressive drug used mainly to lower the risk of organ rejection after allogeneic organ transplant. Adverse effects of FK-506 can prompt patients to end treatment despite the efficacy. In the present study, we investigated the protective effect and mechanism of tetrahydrocurcumin (THC) on FK506-induced renal damage, apoptosis, and oxidative stress to evaluate its possible use for kidney protection.Materials and MethodsThe effect of THC on FK506-induced kidney cell damage was investigated in LLC-PK1 cells. LLC-PK1 cells were pretreated with THC at concentrations of dose for 2 hours followed by addition of FK506 for 24 hours. LLC-PK1 cells were treated with FK506 and THC, and cell viability and glutathione was measured. The number of apoptotic cells was measured using an annexin V/propidium iodide staining with flow cytometry. The effect of apoptosis by THC in LLC-PK1 cells was determined by measuring the caspase-9, caspase-3, B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein levels using Western blotting analyses.ResultsFK506-induced LLC-PK1 renal cell damage was markedly ameliorated by THC treatment. THC protected LLC-PK1 cells by preventing FK506-induced glutathione decrease. THC protects against FK506-induced apoptosis in LLC-PK1 cells. Apoptosis was significantly decreased, and Bcl-2 was elevated in the THC-treated group. Bcl-2-associated X protein, caspase-3, and caspase-9 were decreased in the THC-treated group.ConclusionThese results collectively provide therapeutic evidence that THC ameliorates the FK506-induced renal damage via antioxidant effect and apoptosis inhibition. |
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