Protective Effect of Eupatilin Against Renal Ischemia-Reperfusion Injury in Mice
- Authors
- Jeong, E. K.; Jang, H. J.; Kim, S. S.; Oh, M. Y.; Lee, D. H.; Eom, D. W.; Kang, K. S.; Kwan, H. C.; Ham, J. Y.; Park, C. S.; Jang, D. S.; Han, D. J.
- Issue Date
- 2015-04
- Publisher
- ELSEVIER SCIENCE INC
- Citation
- TRANSPLANTATION PROCEEDINGS, v.47, no.3, pp.757 - 762
- Abstract
- Background. Eupatilin, a pharmacologically active flavone derived from Artemisia species, is known to have antioxidant and anti-inflammatory activities. Ischemia-reperfusion injury (IRI) is a major complication after renal transplantation, with inflammatory responses to IRI exacerbating the resultant renal injury. In the present study, we investigated whether eupatilin exhibits renoprotective activities against ischemia-reperfusion-induced acute kidney injury in mice. Materials and Methods. Renal IRI was induced in male C57BL/6 mice by bilateral renal pedicle occlusion for 30 minutes followed by reperfusion for 48 hours. Eupatilin (10 mg/kg body weight p.o.) was administered 4 days before IRI. Results. Treatment with eupatilin significantly decreased neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 levels in urine, blood urea nitrogen level, and serum creatinine levels, as well as kidney tubular injury. Western blotting indicated that eupatilin significantly increased the levels of heat shock protein 70 and B-cell lymphoma protein, and it attenuated inducible nitric oxide synthase, Bcl-2 associated X protein, and caspase-3 levels 48 hours after IRI. Conclusion. Our findings suggest that eupatilin is a promising therapeutic agent against acute ischemia-induced renal damage.
- Keywords
- ACUTE KIDNEY INJURY; APOPTOSIS; INFLAMMATION; FAILURE; CELLS; NECROSIS; STRESS
- ISSN
- 0041-1345
- URI
- https://pubs.kist.re.kr/handle/201004/125565
- DOI
- 10.1016/j.transproceed.2014.12.044
- Appears in Collections:
- KIST Article > 2015
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