神经保护
自噬
脂质代谢
氧化应激
脂滴
帕金森病
神经退行性变
多巴胺能
细胞生物学
药理学
化学
生物
神经科学
医学
生物化学
多巴胺
疾病
细胞凋亡
内科学
作者
Jesús Alarcón-Gil,Ana Sierra‐Magro,José Á. Morales-García,Marina Sanz-SanCristóbal,Sandra Alonso‐Gil,Marta Cortés‐Canteli,Mireia Niso‐Santano,Guadalupe Martínez-Chacón,José M. Fuentes,Ángel Santos,Ana Pérez‐Castillo
出处
期刊:Cells
[Multidisciplinary Digital Publishing Institute]
日期:2022-07-26
卷期号:11 (15): 2297-2297
被引量:37
标识
DOI:10.3390/cells11152297
摘要
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease after Alzheimer’s disease. The principal pathological feature of PD is the progressive loss of dopaminergic neurons in the ventral midbrain. This pathology involves several cellular alterations: oxidative stress, mitochondrial dysfunction, loss of proteostasis, and autophagy impairment. Moreover, in recent years, lipid metabolism alterations have become relevant in PD pathogeny. The modification of lipid metabolism has become a possible way to treat the disease. Because of this, we analyzed the effect and possible mechanism of action of linoleic acid (LA) on an SH-SY5Y PD cell line model and a PD mouse model, both induced by 6-hydroxydopamine (6-OHDA) treatment. The results show that LA acts as a potent neuroprotective and anti-inflammatory agent in these PD models. We also observed that LA stimulates the biogenesis of lipid droplets and improves the autophagy/lipophagy flux, which resulted in an antioxidant effect in the in vitro PD model. In summary, we confirmed the neuroprotective effect of LA in vitro and in vivo against PD. We also obtained some clues about the novel neuroprotective mechanism of LA against PD through the regulation of lipid droplet dynamics.
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