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Ethics code: IR.MUMS.MEDICAL.REC.1400.715
چکیده: (3 مشاهده)
Background and Objectives: Doxorubicin (Dox) is used in chemotherapy, but its usage is restricted due to cardiotoxicity. Sanguisorba minor (S. minor) and chlorogenic acid (CGA) exhibit pharmacological activities, including the reduction of oxidative stress and induction of programmed cell death. In this investigation, the cardioprotective effects of S. minor and CGA were evaluated following Dox-stimulated toxicity in rats.
Materials and methods: Forty male Wistar rats were used in this research. Saline was administered to the control group; Dox (2.5 mg/kg, intraperitoneally, on alternate days) was injected to the toxicity group; In the second week, groups III and IV received oral S. minor extract at 100 or 300 mg/kg; and Group V received CGA (40 mg/kg, intraperitoneally). Serum levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) were quantified as cardiac injury markers. Cardiac tissues were analyzed for superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and thiol content. The modification of histopathology was studied via hematoxylin and eosin (H&E) staining.
Results: Dox increased LDH, CK-MB, and MDA levels and reduced SOD and thiols. The administration of S. minor and CGA ameliorated Dox-induced biochemical changes. Histopathological analysis demonstrated extracellular edema, moderate congestion, and localized hemorrhage following Dox exposure. These effects were mitigated by treatment with S. minor and CGA.
Conclusion: The administration of S. minor and CGA provided significant protection against Dox-related cardiotoxicity, likely through the modulation of oxidative stress pathways and preservation of myocardial structure.
Materials and methods: Forty male Wistar rats were used in this research. Saline was administered to the control group; Dox (2.5 mg/kg, intraperitoneally, on alternate days) was injected to the toxicity group; In the second week, groups III and IV received oral S. minor extract at 100 or 300 mg/kg; and Group V received CGA (40 mg/kg, intraperitoneally). Serum levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) were quantified as cardiac injury markers. Cardiac tissues were analyzed for superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and thiol content. The modification of histopathology was studied via hematoxylin and eosin (H&E) staining.
Results: Dox increased LDH, CK-MB, and MDA levels and reduced SOD and thiols. The administration of S. minor and CGA ameliorated Dox-induced biochemical changes. Histopathological analysis demonstrated extracellular edema, moderate congestion, and localized hemorrhage following Dox exposure. These effects were mitigated by treatment with S. minor and CGA.
Conclusion: The administration of S. minor and CGA provided significant protection against Dox-related cardiotoxicity, likely through the modulation of oxidative stress pathways and preservation of myocardial structure.
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