Attenuation of DOX‐Associated Biochemical and Histological Brain Alterations

FIGURE 1. Boxplots of (A) acetylcholinesterase (AChE), (B) interleukin 1β (IL‐1β) and (C) interleukin 6 (IL‐6) with whisker bars and median lines of control, allicin (AC), L‐carnitine (LC), doxorubicin (DOX), AC+DOX combination, LC+DOX combination and AC+LC+DOX combination groups. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. Values are reported as mean ± SD (n = 7 samples/group).

FIGURE 2. Boxplots of (A) malondialdehyde (MDA), (B) nitric oxide (NO), (C) superoxide dismutase (SOD), (D) catalase (CAT) and (E) glutathione (GSH) with whisker bars and median lines of control, allicin (AC), L‐carnitine (LC), doxorubicin (DOX), AC+DOX combination, LC+DOX combination and AC+LC+DOX combination groups. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. Values are reported as mean ± SD (n = 7 samples/group).

FIGURE 3. Histopathological analysis of the cerebral cortex following exposure to doxorubicin, illustrating distinct architectural differences among treatment groups: control, allicin (AC), L‐carnitine (LC), doxorubicin (DOX), AC+DOX combination, LC+DOX combination, and AC+LC+DOX combination. The figures were control (A), allicin (B), L‐carnitine (C), doxorubicin (D–F), doxorubicin/allicin (G), doxorubicin/L‐carnitine (H) and doxorubicin/allicin/L‐carnitine (I) groups. The control group maintained normal brain architecture with well‐defined neuronal cells and glial cells. Doxorubicin‐treated groups exhibited significant pathological changes, including neuronal degeneration, neuropil vacuolization and pyknotic nuclei. Treatment with allicin and L‐carnitine, either alone or in combination, showed varying degrees of neuroprotection. Yellow arrow = pyramidal cells, orange arrow = neuroglia, white arrow = granule cell, red arrow = congestion and haemorrhage, blue arrow = vacuolation, green arrow = denatured cell.

FIGURE 4. Histopathological analysis of the cerebellum following exposure to doxorubicin, demonstrating architectural differences across treatment groups: control, allicin (AC), L‐carnitine (LC), doxorubicin (DOX), AC+DOX combination, LC+DOX combination and AC+LC+DOX combination. The figures were control (A), allicin (B), L‐carnitine (C), doxorubicin (D–F), doxorubicin/allicin (G), doxorubicin/L‐carnitine (H) and doxorubicin/allicin/L‐carnitine (I) groups. The control group exhibited normal cerebellar architecture with well‐defined Purkinje cells and granule cells. Doxorubicin‐treated groups showed significant pathological changes, including neuronal degeneration and vacuolization. Treatment with allicin and L‐carnitine, either alone or in combination, mitigated these pathological changes to varying extents. White arrow = normal structures, black arrow = degeneration and necrosis.

FIGURE 5. Histopathological analysis of the hippocampus following exposure to doxorubicin, highlighting architectural differences among treatment groups: control, allicin (AC), L‐carnitine (LC), doxorubicin (DOX), AC+DOX combination, LC+DOX combination and AC+LC+DOX combination. The figures were control (A), allicin (B), L‐carnitine (C), doxorubicin (D–F), doxorubicin/allicin (G), doxorubicin/L‐carnitine (H) and doxorubicin/allicin/L‐carnitine (I) groups. The control group maintained typical hippocampal architecture with well‐defined layers, including the molecular layer, pyramidal cell layer and polymorphic layer. Doxorubicin‐treated groups exhibited significant neuronal degeneration, vacuolization and disorganization of hippocampal layers. Treatment with allicin and L‐carnitine, either alone or in combination, showed considerable preservation of hippocampal structure, suggesting potential co‐administration protective effects against doxorubicin‐induced damage. The black arrow indicates degenerative signs characterized by disordered arrangement, dilated intercellular spaces and karyopyknosis.