Tavakoli Maedeh, Mohammadi Negin, Barzegar Mohsen, Valian Neda, Hosseinmardi Narges, Sahari Mohammad Ali, Saremi Sabereh
Department of Food Science and Technology Tarbiat Modares University Tehran Iran.
Neuroscience Research Center Shahid Beheshti University of Medical Sciences Tehran Iran.
Food Sci Nutr. 2025 May 16;13(5):e70204. doi: 10.1002/fsn3.70204. eCollection 2025 May.
Pistachio green hull extract (PGHE), an agro-industrial by-product, is rich in phenolic compounds with significant inherent antioxidant and anti-inflammatory activities. In this study, the neuroprotective effects of PGHE against Parkinson's disease (PD), a progressive neurodegenerative disorder, were evaluated both in vivo and in vitro. The lethal dose (LD) of PGHE was greater than 5000 mg/kg, indicating its safety and nontoxicity. Rats were orally treated with PGHE (800 mg/kg/day) 24 h after injection of 6-OHDA (20 μg/rat in right MFB) for 14 days. Motor function was evaluated on Days 7 and 15 after 6-OHDA administration using the cylinder, narrow beam, pole, rotarod, and apomorphine-induced rotations tests. PGHE significantly improved motor impairments induced by 6-OHDA. An in vitro study indicated that increasing concentrations of PGHE up to 250 μg/mL resulted in a reduction in the aggregation of α-synuclein characterized by thioflavin T fluorescence and Congo red assays. Transmission electron microscopy images further confirmed a decrease in α-synuclein aggregation in the presence of PGHE. In conclusion, these findings indicated that PGHE improved motor deficits in a rat model of PD and decreased α-synuclein aggregation in vitro, suggesting that it can be considered a novel dietary supplement for PD therapy. However, more studies are needed to clarify the underlying mechanisms of PGHE's effect on PD pathogenesis and its potential applications in developing functional foods or nutraceuticals.
开心果绿壳提取物（PGHE）是一种农业工业副产品，富含具有显著固有抗氧化和抗炎活性的酚类化合物。在本研究中，对PGHE针对帕金森病（PD，一种进行性神经退行性疾病）的神经保护作用进行了体内和体外评估。PGHE的致死剂量（LD）大于5000 mg/kg，表明其安全性和无毒性。在注射6-羟基多巴胺（6-OHDA，20μg/只大鼠，右侧内侧前脑束）24小时后，大鼠口服PGHE（800 mg/kg/天），持续14天。在给予6-OHDA后的第7天和第15天，使用圆筒、窄梁、杆、转棒和阿扑吗啡诱导旋转试验评估运动功能。PGHE显著改善了6-OHDA诱导的运动障碍。一项体外研究表明，PGHE浓度增加至250μg/mL可导致以硫黄素T荧光和刚果红测定为特征的α-突触核蛋白聚集减少。透射电子显微镜图像进一步证实了在PGHE存在下α-突触核蛋白聚集减少。总之，这些发现表明PGHE改善了PD大鼠模型的运动缺陷，并在体外减少了α-突触核蛋白聚集，表明它可被视为一种用于PD治疗的新型膳食补充剂。然而，需要更多的研究来阐明PGHE对PD发病机制影响的潜在机制及其在开发功能性食品或营养保健品中的潜在应用。
