Tungalag Tsendsuren, Yang Dong Kwon
Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Jeonbuk National University, Iksan, Jeollabuk-do 54596, Korea.
Biomedicines. 2021 Mar 13;9(3):295. doi: 10.3390/biomedicines9030295.
Parkinson's disease (PD) is characterized by progressive dopaminergic neuron loss or dysfunction and is the second most prevalent neurodegenerative disorder after Alzheimer's disease. However, current therapeutic strategies for PD are limited to treating the outcomes of this disease rather than preventing it. Sinapic acid (SA) is a phenolic compound with potential antioxidant properties, which reportedly acts as a therapeutic agent against many diseases including cancer, as well as cardiac and liver diseases. However, little is known about the effects of SA against neurodegenerative disorders. Therefore, our study sought to evaluate the neuroprotective effects of non-cytotoxic concentrations of SA against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in SH-SY5Y human neuroblastoma cells, which we used as an in vitro PD model. SA increased cell viability and rescued the cells from 6-OHDA-induced apoptotic cell death. Additionally, oxidative stress responses were significantly blocked by SA, including reactive oxygen species (ROS) overproduction and decreased expression levels of antioxidant proteins. Notably, SA also attenuated mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Moreover, SA dramatically inhibited the activation of mitogen-activated protein kinase (MAPK) proteins. Taken together, our findings highlight the potential PD prevention effects of SA, as well as its underlying mechanisms, making this compound a promising prevention and treatment agent for PD.
帕金森病(PD)的特征是多巴胺能神经元进行性丧失或功能障碍,是仅次于阿尔茨海默病的第二大常见神经退行性疾病。然而,目前针对PD的治疗策略仅限于治疗该疾病的后果,而非预防。芥子酸(SA)是一种具有潜在抗氧化特性的酚类化合物,据报道可作为治疗包括癌症以及心脏和肝脏疾病在内的多种疾病的药物。然而,关于SA对神经退行性疾病的影响知之甚少。因此,我们的研究旨在评估非细胞毒性浓度的SA对6-羟基多巴胺(6-OHDA)诱导的SH-SY5Y人神经母细胞瘤细胞神经毒性的神经保护作用,我们将其用作体外PD模型。SA提高了细胞活力,并使细胞从6-OHDA诱导的凋亡性细胞死亡中获救。此外,SA显著阻断了氧化应激反应,包括活性氧(ROS)过量产生和抗氧化蛋白表达水平降低。值得注意的是,SA还减轻了线粒体功能障碍和内质网(ER)应激。此外,SA显著抑制了丝裂原活化蛋白激酶(MAPK)蛋白的激活。综上所述,我们的研究结果突出了SA对PD的潜在预防作用及其潜在机制,使该化合物成为一种有前景的PD预防和治疗药物。