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<p>This study aimed to evaluate the protective and therapeutic effects of Cinnamon Bark Oil (CBO) on cerebral ischemia/reperfusion (I/R) injury in rats. The focus was on its potential antioxidant, anti-inflammatory, and antiapoptotic properties. Forty-four female <i>Wistar albino</i> rats were divided into four groups: Sham + CBO group, I/R + Vehicle group, prophylactic (CBO + I/R) group and therapeutic (I/R + CBO) group. Bilateral common carotid artery occlusion was performed to induce ischemia, followed by reperfusion for 72&#xa0;h. CBO (100&#xa0;mg/kg) was administered orally. Biochemical, histopathological, and immunohistochemical analyses were conducted, measuring oxidative stress markers, inflammatory cytokines, and neuronal degeneration in the cerebral cortex and hippocampus. Histopathological analysis revealed that CBO significantly reduced neuronal degeneration in both the prophylactic and therapeutic groups. Biochemically, CBO increased superoxide dismutase (SOD) and total antioxidant capacity (TAC), while decreasing malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF-α) levels. Immunohistochemical staining showed decreased apoptotic markers (caspase-3, Bax) in the prophylactic and therapeutic groups. CBO demonstrated neuroprotective effects in cerebral I/R injury through its antioxidant, anti-inflammatory, and antiapoptotic properties. These findings suggest its potential as a complementary therapeutic agent for ischemic brain injuries.</p>

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The effect of cinnamon bark oil in bilateral common carotid artery occlusion-induced cerebral ischemia model in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月12日

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  • Melike Aba,
  • Yuksel Kablan,
  • Onural Ozhan,
  • Elif Karaca,
  • Ahmet Ulu,
  • Burhan Ates,
  • Nigar Vardi,
  • Hakan Parlakpinar

摘要

This study aimed to evaluate the protective and therapeutic effects of Cinnamon Bark Oil (CBO) on cerebral ischemia/reperfusion (I/R) injury in rats. The focus was on its potential antioxidant, anti-inflammatory, and antiapoptotic properties. Forty-four female Wistar albino rats were divided into four groups: Sham + CBO group, I/R + Vehicle group, prophylactic (CBO + I/R) group and therapeutic (I/R + CBO) group. Bilateral common carotid artery occlusion was performed to induce ischemia, followed by reperfusion for 72 h. CBO (100 mg/kg) was administered orally. Biochemical, histopathological, and immunohistochemical analyses were conducted, measuring oxidative stress markers, inflammatory cytokines, and neuronal degeneration in the cerebral cortex and hippocampus. Histopathological analysis revealed that CBO significantly reduced neuronal degeneration in both the prophylactic and therapeutic groups. Biochemically, CBO increased superoxide dismutase (SOD) and total antioxidant capacity (TAC), while decreasing malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF-α) levels. Immunohistochemical staining showed decreased apoptotic markers (caspase-3, Bax) in the prophylactic and therapeutic groups. CBO demonstrated neuroprotective effects in cerebral I/R injury through its antioxidant, anti-inflammatory, and antiapoptotic properties. These findings suggest its potential as a complementary therapeutic agent for ischemic brain injuries.