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The licorice ( Glycyrrhiza glabra ) root extract alleviated TCDD‐induced toxicity in primary rat hepatocytes (975.5)
Author(s) -
Chu Xiaoting,
Cruz Joseph,
Hwang Seong Gu
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.975.5
Subject(s) - toxicity , hepatocyte , chemistry , viability assay , antioxidant , pharmacology , glycyrrhiza , cytochrome p450 , biochemistry , biology , cell , in vitro , enzyme , medicine , pathology , alternative medicine , organic chemistry
2, 3, 7, 8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) is the most toxic member of a class of planar, halogenated aromatic hydrocarbons. Recently it raises great public concern about its impact on human health. It has been suggested that TCDD induce hepatocyte toxicity by a mechanism involving generation of ROS through CYP1A1 (cytochrome P450 1A1) activation. Many studies indicated that licorice ( Glycyrrhiza glabra ) root extract (LRE) exhibits chemopreventive and detoxicative properties. The aim of this study was to assess the effect of ethanolic LRE against TCDD induced toxicity in a primary culture of rat hepatocytes. Primary cultured hepatocytes were treated with TCDD (10nM) alone or together with LRE (0‐400μg/ml) for 24 and 48 hours. Treatment with TCDD alone lowered cell viability, but the toxic effect of TCDD on cell viability was recovered by the treatment of LRE dose dependently. Antioxidant capability by DPPH assay showed that LRE have a strong antioxidant activity. RT‐PCR and Western Blot analysis both showed that TCDD toxicity related genes (AhR, ARNT and CYP1A1) were subsequently down‐regulated by LRE treatment in a dose dependent manner. DNA fragmentation assay showed the protective effect of LRE against TCDD mediated DNA damage. These data suggested that LRE can mitigate TCDD toxicity in cultured hepatocytes by strong antioxidant activity as well as the suppression of CYP1A1 expression followed by down regulation of AhR and ARNT genes. In conclusion, LRE can be used as a potential toxicity alleviating agent against TCDD induced hepatocyte toxicity.