Title of article :
Mitigation of 5-Fluorouracil induced renal toxicity by chrysin via targeting oxidative stress and apoptosis in wistar rats
Author/Authors :
Rashid، نويسنده , , Summya and Ali، نويسنده , , Nemat and Nafees، نويسنده , , Sana and Hasan، نويسنده , , Syed Kazim and Sultana، نويسنده , , Sarwat، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
9
From page :
185
To page :
193
Abstract :
5-Fluorouracil (5-FU) is a potent antineoplastic agent commonly used for the treatment of various malignancies. It has diverse adverse effects such as cardiotoxicity, nephrotoxicity and hepatotoxicity which restrict its wide and extensive clinical usage. It causes marked organ toxicity coupled with increased oxidative stress and apoptosis. Chrysin (CH), a natural flavonoid found in many plant extracts, propolis, blue passion flower. It has antioxidative and anti-cancerous properties. The present study was designed to investigate the protective effects of CH against 5-FU induced renal toxicity in wistar rats using biochemical, histopathological and immunohistochemical approaches. ere subjected to prophylactic oral treatment of CH (50 and 100 mg/kg b.wt.) for 21 days against renal toxicity induced by single intraperitoneal administration of 5-FU (150 mg/kg b.wt.). The possible mechanism of 5-FU induced renal toxicity is the induction of oxidative stress; activation of apoptotic pathway by upregulation of p53, bax, caspase-3 and down regulating Bcl-2. However prophylactic treatment of CH decreased serum toxicity markers, increased anti-oxidant armory as well as regulated apoptosis in kidney. Histopathological changes further confirmed the biochemical and immunohistochemical results. Therefore, results of the present finding suggest that CH may be a useful modulator in mitigating 5-FU induced renal toxicity.
Keywords :
CH , 5-FU , oxidative stress , apoptosis , KIM-1
Journal title :
Food and Chemical Toxicology
Serial Year :
2014
Journal title :
Food and Chemical Toxicology
Record number :
2126866
Link To Document :
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