Effects of Cyclosporine and Azacitidine on Some Hematologic and Biochemical Parameters of Benzene-Induced Aplastic Anemia in Rats
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Abstract
Aplastic anemia, marked by deficiencies in hematopoietic stem cells, leads to peripheral blood pancytopenia and hypocellular bone marrow. This study aimed to evaluate the therapeutic efficacy of cyclosporine and azacitidine, administered either alone or in combination, in rats with benzene-induced aplastic anemia, focusing on restoring normal blood cell levels and preventing disease complications. Thirty adult female Wistar rats (Rattus norvegicus) were randomly divided into five groups: negative control (C-, untreated), positive control (C+, induced aplastic anemia with distilled water), cyclosporine-treated (CsA, 5.86 mg/kg), azacitidine-treated (Aza, 5.75 mg/kg), and combination-treated (CsA+Aza, 3.68 mg/kg each). Benzene (1940 mg/kg) was administered orally for fifteen days to induce aplastic anemia. Post a 30-day treatment period, evaluations included differential WBC and reticulocyte counts, serum IL-2 levels, and alkaline phosphatase (ALP) activity. Results showed significant improvements in WBC% and reticulocyte% in all treated groups compared to the C+ group, with the combination-treated group showing the highest enhancement. IL-2 levels in the combination group were significantly reduced compared to other treatment groups, aligning closely with the negative control. The ALP activity was significantly higher in both the cyclosporine and azacitidine-treated groups compared to the positive control, with the combination group showing a marked increase over the azacitidine group but no significant difference from the cyclosporine group and negative control. In conclusion, the study demonstrates the potential therapeutic benefits of cyclosporine and azacitidine in treating benzene-induced aplastic anemia in rats. The combination therapy, in particular, showed improved efficacy in all tested parameters, suggesting a potential strategy for dose reduction and toxicity mitigation.
Received: 28 April 2023
Revised : 24 June 2023
Accepted: 23 July 2023
Published: 28 December 2023
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