Cadmium (Cd) is a widespread toxic pollutant of occupational and environmental concern because of its diverse toxic effects including hepatotoxicity, nephrotoxicity and reproductive toxicities. There is an increasing demand for herbal medicines. Licorice is a plant used in traditional medicine across the world effectively used as an anti-oxidant. Aim: Investigate the protective role of licorice against cadmium chloride (CdCl2) induced hepatotoxicity. Methods: Forty male albino rats were randomly divided into four groups each consisting of 10 animals and were treated as follows: Untreated control group (G1), Licorice treated group (300mg/ kg b.w) intragastric daily for 21 days (G2), CdCl2 treated group (3mg/kg b.w) intraperitoneal 5 times per week for 3 weeks (G3) and a group treated with the licorice (300mg/ kg b.w) intragastric for 3days before CdCl2 injection and continued along with CdCl2 injection (3 mg/kg b.w) 5 times per week for 3 weeks (G4). Specimens from liver were taken and examined histopathologically besides estimation of hepatic enzymatic functions. Also, immunohistochemical expression of B-cell lymphoma 2 (Bcl-2) in the livers of all experimental rats was investigated. Results: Significant increase of hepatic enzymes levels in Cd treated rats when compared with control group with low levels of albumin and total protein. While, co-treatment of CdCl2 with licorice reduces the elevation of enzymatic activities. Histopathologically, the liver sections from Cd group showed severe changes including marked degenerative changes of hepatic cells, dark stained nuclei with condensed cytoplasm indicating nuclear pyknosis accompanied with marked kupffer cells proliferation as well as focal areas of hepatic necrosis with mononuclear cells infiltration. Combined administration of Licorice with CdCl2 improves the biochemical and histopathological changes induced by cadmium intoxication. Down-regulation of Bcl-2 in hepatic cells induced by Cd was restored by co-administration of licorice. Conclusion: Licorice has a protective effect against hepatotoxicity of cadmium.