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    <subfield code="a">The efficiency of andrographolide in attenuating cadmium-induced hepatotoxicity in rats</subfield>
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    <subfield code="a">The aim of this study was to determine the efficiency of andrographolide (AP) in attenuating cadmium-induced hepatotoxicity in rats in comparison with silymarin (SL), a standard hepatoprotective agent. Rats were treated with CdCl&#x2082; at doses of 0.75, 1.0 mg/kg, intraperitoneal injection (i.p.), for 14 days. For the next 7 days, rats were given oral doses of AP at 6 (AP6), 60 (AP60) mg/kg, and SL at 60 (SL60) mg/kg. The significant decrease of body weight was observed in all Cd-treated rats during the first 14 days and then increased gradually during the drug treatments. Intraperitoneal injection of CdCl&#x2082; had higher levels of cadmium accumulated in liver than kidney. Moreover, Cadmium accumulation also increased in lung, brain and testis of cadmium-treated rats. In Cd0.75-treated group, AP60 significantly decreased Cd accumulation in kidney while this effect was not significant in liver. However, in the Cd1.0-treated group, AP60 and SL60 significantly decreased Cd accumulation in liver. In addition, these drug treatments (AP60 and SL60) could also decrease Cd accumulation in kidney. Administration of AP60 and SL60 may possibly increase cadmium excretion resulting in the reduction of cadmium accumulation in liver and kidney of cadmium-treated rats. All Cd-treated rats showed histopathological changes in liver. The results from liver function test showed that alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities of Cd1.0-treated rats increased significantly. Both AP and SL at 60 mg/kg seemed to decrease these liver enzyme activities induced by cadmium whereas AP at 6 mg/kg did not show this effect. Post-treatment of AP and SL (60 mg/kg) for 7 days was found to attenuate hepatotoxicity induced by CdCl&#x2082;. However, AP at the dose 6 mg/kg had no hepatoprotective effect on cadmium-induced hepatic damage. The present results indicated that AP60 is as potent as SL60 for the treatment of hepatotoxicity induced by cadmium. Therefore, AP may have the potential to be used as a hepatoprotective drug against Cd-induced toxicity</subfield>
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