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C‐Phycocyanin ameliorates 2‐acetylaminofluorene induced oxidative stress and MDR1 expression in the liver of albino mice
Author(s) -
Roy Karnati R.,
Nishanth Reddy P.,
Sreekanth Devalraju,
Reddy Gorla Venkateswara,
Reddanna Pallu
Publication year - 2008
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2007.00290.x
Subject(s) - 2 acetylaminofluorene , oxidative stress , oxidative phosphorylation , chemistry , microbiology and biotechnology , medicine , biology , enzyme , biochemistry , microsome
Aim: To study the effect of C‐Phycocyanin (C‐PC), a biliprotein isolated from Spirulina platensis , on 2‐acetylaminofluorene (2‐AAF) induced oxidative stress and MDR1 expression in the liver of albino mice. Methods: In the present study, albino mice aged 40–60 days were used. The mice were randomly assigned to four groups of six animals each. The first group was treated with the vehicle (absolute alcohol), the second group was treated with C‐PC (50 mg/kg body weight), the third group was treated with 2‐AAF (25 mg/kg body weight) and the fourth group was treated with C‐PC (50 mg/kg body weight) and 2‐AAF, daily for 3 days. The mice were sacrificed and the tissues were collected and stored for histology and biochemical studies. Results: 2‐AAF induced liver tissue damage in albino mice. 2‐AAF treatment resulted in upregulation of MDR1 expression and enhanced the generation of reactive oxygen species (ROS). It also induced phosphorylation of Akt and nuclear translocation of NF‐κB. Co‐administration of C‐PC and 2‐AAF inhibited the expression of MDR1 by preventing ROS generation, Akt phosphorylation and NF‐κB nuclear translocation. Conclusion: 2‐AAF‐induced oxidative stress is reduced by C‐PC treatment. C‐PC inhibited the 2‐AAF induced expression of MDR1 by interfering at the level of ROS generation, Akt phosphorylation and NF‐κB translocation. This study reveals the usefulness of C‐PC in preventing oxidative stress and downregulation of MDR1 induced by xenobiotics like 2‐AAF.