Renoprotective effects of the methanolic extract of Tanacetum parthenium against carbon tetrachloride-induced renal injury in rats

Document Type : Original Research Article

Authors

1 Department of Biochemistry, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran

2 Department of Pathology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran

3 Department of Physiology, Ardabil University of Medical Sciences, Ardabil, Iran

4 Department of Health Information Technology Management, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran

Abstract

Objective: Studies have demonstrated that carbon tetrachloride (CCl4) increases the generation of reactive oxygen species (ROS) in many tissues including the kidney, heart, lung, brain, and liver. The major aim of the present study was to evaluate the protective activity of Tanacetum parthenium extract (TPE) in renal tissues of CCl4-intoxicated rats.
Materials and Methods: Animals were divided into seven groups of six rats. Group 1 was the control group that was not treated with CCl4. The rats in the other groups were intraperitoneally injected with CCl4 (1.5 ml/kg, 1:1 in olive oil) on day 14. Rats in the groups bTPE40, bTPE80, and bTPE120 were gavaged with 40, 80, and 120 mg/kg of TPE, respectively for 14 constitutive days on a daily basis, before CCl4 administration. Rats in groups aTPE80 and aTPE120 were gavaged with 80 and 120 mg/kg of TPE, respectively, 2, 6, 24 and 48 hr after receiving CCl4. Blood samples were collected at the end of the 16th day through an intracardiac puncture and then serums were separated.
Results: CCl4 increased urea, creatinine, uric acid and creatinine: albumin (C/A) ratio level in serum and decreased total antioxidant and antioxidant enzymes (SOD and GPx) when compared to the control group (p<0.001). But administration of TPE to rats either before or after exposure to CCl4, attenuated these changes when compared with CCl4 control group (p Conclusion: TPE had potent nephroprotective effects against oxygen free radicals produced through CCl4 metabolism.

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