Abstract: Background and Objective: Cisplatin is considered one of the most effective and widely used anti-neoplastic drugs in chemotherapeutic regimes of cancer treatment. Toxic side effects associated with cisplatin including nephrotoxicity, neurotoxicity, hepatotoxicity and bone marrow toxicity, were limit its clinical uses. Nowadays, researchers were directed to use herbal medicine to overcome these side effects. Silymarin is one of herbal medicine which has anti-oxidant, anti-apoptotic and anti-inflammatory effects. This study was designed to investigate the efficacy of silymarin against hematological and pathological disorders, bone marrow toxicity and hepatotoxicity induced by cisplatin in rats. Materials and Methods: Thirty-two Albino rats were used and were divided into 4 equal groups as follow; control, silymarin-treated, cisplatin-treated and silymarin-protected group. The experiment continued for thirteen days through which blood and tissue samples were taken at 8th and 13th days of the experiment. Hematological evaluation includes: RBCs count, packed cell volume, hemoglobin concentration, platelets countas well as total and differential leukocytic counts. Bone marrow evaluation was done through applying the differential cell count, cellular density, myeloid/erythroid ratio, megakaryocyte percent and maturation index for both myeloid and erythroid series. Hepatic biomarkers were investigated including activities of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase. Cytological and histopathological examinations were also performed on all hepatic sections. The collected data were analyzed by one-way analysis of variance (ANOVA). Results: Cisplatin-treated group showed normocytic normochromic anemia with marked suppression in bone marrow cell proliferation manifested by diminishing of maturation indices in association with megakaryocyte hypoplasia. Elevated hepatic biomarkers in association with cytological findings in cisplatin-treated group documented the occurrence of severe hepatic lipidosis. Immunohistochemistry revealed hepatic toxicity through activation of caspase-3 and inhibition of anti-nuclear factor kappa beta activation in hepatocellular nuclei of cisplatin treated group. In silymarin protected group, most of hematological alterations, hepatic biomarkers as well as cytological and histopathological changes were significantly improved (p<0.05)toward control levels. Conclusion: It is concluded that prior-treatment with silymarin partially attenuated the cisplatin induced anemia, thrombocytopenia, bone marrow myelosuppression and hepatotoxicity through its anti-apoptotic and cytoprotective properties.