The Effect of Alpha-pinene on Amyloid-beta-induced Neuronal Death and Depression in Male Wistar Rats

Mohammad-Kazem Khan-Mohammadi-Khorrami, M. Asle-Rousta, M. Rahnema, Rahim Amini
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引用次数: 3

Abstract

Background & objectives: The deposition of amyloid beta (Aβ) peptide in the brain is one of the most important features of Alzheimer's disease. In addition to memory loss, Aβ can lead to depression behavior. Alpha-pinene is a type of monoterpene that has antioxidant, antiinflammatory, and neuroprotective effects. Here, by using an animal model for Alzheimer's disease, we investigated the effect of alpha-pinene on neuronal cell death in the hippocampus and depression induced by Aβ1-42. Methods: Male Wistar rats weighing 240-260 g were divided into four groups including control, alpha-pinene, Aβ, and Aβ-alpha-pinene. Rats were placed in stereotaxic surgery apparatus and Aβ1-42 was injected into the hippocampus (4 μg per side) and alpha-pinene was treated intraperitoneally (50 mg/kg) for 14 consecutive days. At the end of the course, the level of depression was assessed using the forced swimming test. The animals' hippocampus was also examined microscopically after Nissl staining. Results: Intra-hippocampal injection of Aβ1-42 increased the total immobility time in the forced swimming test (p<0.01), decreased the number of pyramidal neurons in the CA1 area (p<0.001), and reduced the thickness of the neuronal layer in this region of the hippocampus. Treatment with alpha-pinene largely prevented these changes. Conclusion: It can be concluded that alpha-pinene decreased the beta-amyloid-induced depressive behavior in rats and inhibited the neuronal loss, suggesting that this neuroprotective compound may have a critical role in depression. Alpha-pinene is probably a suitable therapeutic strategy for repressing Aβ-induced neurodegeneration.
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α -蒎烯对β -淀粉样蛋白诱导的雄性Wistar大鼠神经元死亡和抑郁的影响
背景与目的:淀粉样蛋白β(Aβ)肽在大脑中的沉积是阿尔茨海默病最重要的特征之一。除了记忆力丧失外,Aβ还会导致抑郁行为。α-蒎烯是一种单萜,具有抗氧化、抗炎和神经保护作用。在这里,通过使用阿尔茨海默病的动物模型,我们研究了α-蒎烯对海马神经元细胞死亡和Aβ1-42诱导的抑郁症的影响。方法:雄性Wistar大鼠体重240-260g,分为四组,包括对照组、α-蒎烯组、Aβ组和Aβ-α-松果烯组。将大鼠置于立体定向手术装置中,将Aβ1-42注射至海马(每侧4μg),并连续14天腹膜内注射α-蒎烯(50mg/kg)。课程结束时,使用强迫游泳测试来评估抑郁程度。Nissl染色后,还对动物的海马进行了显微镜检查。结果:在强迫游泳试验中,海马内注射Aβ1-42增加了总不动时间(p<0.01),减少了CA1区锥体神经元的数量(p<0.001),并减少了海马该区神经元层的厚度。α-蒎烯治疗在很大程度上阻止了这些变化。结论:α-蒎烯降低了β-淀粉样蛋白诱导的大鼠抑郁行为,抑制了神经元的丢失,提示该神经保护化合物可能在抑郁症中发挥关键作用。α-蒎烯可能是抑制aβ诱导的神经退行性变的合适治疗策略。
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