Open AccessChicory (Cichorium intybus L.) Root Extract Regulates the Oxidative Status and Antioxidant Gene Transcripts in CCl4-Induced Hepatotoxicity
Author(s) -
Yasser S. ElSayed,
Mohamed A. Lebda,
Mohammed Hassinin,
Saad A. Neoman
Publication year - 2015
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0121549
Subject(s) - cichorium , antioxidant , glutathione reductase , glutathione peroxidase , oxidative stress , lipid peroxidation , glutathione , chemistry , malondialdehyde , pharmacology , liver injury , biochemistry , catalase , biology , enzyme , botany
The ability of Cichorium intybus root extract (chicory extract) to protect against carbon tetrachloride (CCl 4 )-induced oxidative stress and hepatotoxicity was evaluated in male rats. The rats were divided into four groups according to treatment: saline (control); chicory extract (100 mg/kg body weight daily, given orally for 2 weeks); CCl 4 (1 ml/kg body weight by intraperitoneal injection for 2 consecutive days only); or chicory extract (100 mg/kg body weight daily for 2 weeks) + CCl 4 injection on days 16 and 17. The levels of hepatic lipid peroxidation, antioxidants, and molecular biomarkers were estimated twenty-four hours after the last CCl 4 injection. Pretreatment with chicory extract significantly reduced CCl 4 -induced elevation of malondialdehyde levels and nearly normalized levels of glutathione and activity of glutathione S-transferase, glutathione peroxidase (GPx), glutathione reductase, catalase (CAT), paraoxonase-1 (PON1), and arylesterase in the liver. Chicory extract also attenuated CCl 4 -induced downregulation of hepatic mRNA expression levels of GPx1 , CAT and PON1 genes. Results of DNA fragmentation support the ability of chicory extract to ameliorate CCl 4 -induced liver toxicity. Taken together, our results demonstrate that chicory extract is rich in natural antioxidants and able to attenuate CCl 4 -induced hepatocellular injury, likely by scavenging reactive free radicals, boosting the endogenous antioxidant defense system, and overexpressing genes encoding antioxidant enzymes.