Berberine attenuates liver damage, hematological, biochemical, and molecular changes induced by cadmium chloride via inflammation, apoptosis, and oxidative stress suppression.

Cadmium (Cd) is a toxic heavy metal widely recognized for its detrimental effects on human and animal health. The liver, a primary organ for detoxification, is particularly susceptible to cadmium-induced damage. Berberine (BBR) is a natural alkaloid extracted from a plant known for its antioxidant and chemoprotective effects on the liver. Twenty-eight Male Wistar rats were divided into four groups: control, berberine (BBR; 150 mg/kg BW/day), cadmium chloride (CdCl2, 1.8 mg/kg BW/day), and BBR+ Cd (Cd after 2 h of BBR administration). Dosages of BBR and CdCl2 were given orally for 21 consecutive days. Rats treated with Cd displayed remarkable changes in hematological parameters, lipid profile, and oxidative stress markers (TBARS, H2O2), and a marked decrease in enzymatic and non-enzymatic antioxidants, transaminases, and alkaline phosphatase activities, and serum protein level. Additionally, Cd administration induced apoptosis and inflammation, in addition to histological abnormalities, in the liver tissue. Otherwise, BBR intake alone significantly reduced lipid peroxidation and improved the antioxidant status. Moreover, supplementation with BBR followed by CdCl2 intoxication restored most of the studied indices compared to the CdCl2 group. In summary, BBR demonstrated its exceptional ability to eliminate CdCl2 toxicity. Because of its antioxidant potential, it may offer a novel approach to treating metal poisoning.