Abbaoui Abdellatif, Gamrani Halima
Cadi Ayyad University, Faculty of Sciences Semlalia, Neurosciences, Pharmacology and Environment Unit, Marrakesh, Morocco.
Cadi Ayyad University, Faculty of Sciences Semlalia, Neurosciences, Pharmacology and Environment Unit, Marrakesh, Morocco.
Acta Histochem. 2018 Aug;120(6):542-550. doi: 10.1016/j.acthis.2018.06.005. Epub 2018 Jun 27.
We aim herein to assess the neurotoxic effects of subchronic Cu-exposition (0125%) for 6 weeks on dopaminergic and astroglial systems then locomotor activity in rats as well as the probable therapeutic efficiency of curcumin-I (30 mg/kg B.W.). We found that intoxicated rats showed a significant impairment of Tyrosine Hydroxylase (TH) within substantia nigra pars compacta (SNc), ventral tegmental area (VTA) and the striatal outputs together with loss expression of GFAP in these structures. This was linked with an evident decrease in locomotor performance. Co-treatment with curcumin-I inverted these damages and exhibited a significant neuroprotective potential, thus, both TH expression and locomotor performance was reinstated in intoxicated rats. These results prove a profound dopaminergic and astroglial damages following subchronic Cu exposition and new beneficial curative potential of curcumin against subchronic Cu-induced astroglial and dopaminergic neurotoxicity. Consequently, we suggest that Cu neurotoxicity may be strengthened in vivo firstly by attacking and weaking the astroglial system, and curcumin could be prized as a powerful and preventive target for the neurodegenerative diseases related metal element, especially Parkinson's disease.
我们旨在评估大鼠连续6周亚慢性暴露于125%铜对多巴胺能和星形胶质细胞系统以及运动活性的神经毒性作用，以及姜黄素I（30mg/kg体重）可能的治疗效果。我们发现，中毒大鼠黑质致密部（SNc）、腹侧被盖区（VTA）和纹状体输出中的酪氨酸羟化酶（TH）显著受损，这些结构中的胶质纤维酸性蛋白（GFAP）表达缺失。这与运动性能的明显下降有关。姜黄素I联合治疗逆转了这些损伤，并表现出显著的神经保护潜力，因此，中毒大鼠的TH表达和运动性能均得以恢复。这些结果证明了亚慢性铜暴露后多巴胺能和星形胶质细胞的严重损伤，以及姜黄素对亚慢性铜诱导的星形胶质细胞和多巴胺能神经毒性的新的有益治疗潜力。因此，我们认为铜神经毒性可能首先通过攻击和削弱星形胶质细胞系统在体内增强，姜黄素可被视为与金属元素相关的神经退行性疾病，尤其是帕金森病的强大预防靶点。
