Peroxisome Proliferator-Activated Receptors: A New Ray Of Hope For Parkinson’s Disease

R. Bhatt, S. Parmar
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Abstract

PD (PD) is a debilitating progressive age-related neurodegenerative disorder that negatively impacts bodily movement. It is the second most common type of neurodegenerative disease after Alzheimer's disease. Although the etiology and pathogenesis of PD remain unknown, a vast body of evidence indicates that oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, and proteasomal dysfunction all play a role in the disease's pathogenesis. Because of the multifactorial nature of the disease, current drug treatment can only offer symptomatic relief and cannot stop or delay the disease progression. The Peroxisome proliferator-activated receptors (PPARs) are the member of the receptor’s superfamily called, nuclear receptors, regulates the growth, differentiation of the tissues, inflammation, mitochondrial function, wound healing, lipid metabolism, and glucose metabolism. Several PPAR agonists have recently been shown to protect neurons from oxidative damage, inflammation, and apoptosis in Alzheimer's disease, PD, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We review the research on the neuroprotective effects of PPAR agonists in in-vitro and in-vivo models of PD in this paper. Similarly, the pharmacological mechanism of PPAR agonists' neuroprotective effects is examined. Finally, PPAR agonists exert neuroprotective effects by controlling the expression of a set of genes involved in cell survival processes, suggesting that they may be a potential therapeutic target in crippling neurodegenerative diseases like PD. Keywords: Parkinson’s disease, neuroprotective, neuro inflammatory, oxidative stress, PPAR agonist
过氧化物酶体增殖物激活受体:帕金森病的新希望
帕金森病(PD)是一种使人衰弱的进行性年龄相关的神经退行性疾病,对身体运动产生负面影响。它是继阿尔茨海默病之后第二常见的神经退行性疾病。虽然PD的病因和发病机制尚不清楚,但大量证据表明,氧化应激、炎症、细胞凋亡、线粒体功能障碍和蛋白酶体功能障碍都在PD的发病机制中发挥作用。由于该疾病的多因素性质,目前的药物治疗只能提供症状缓解,不能阻止或延缓疾病进展。过氧化物酶体增殖激活受体(PPARs)是受体超家族的成员,被称为核受体,调节生长,组织分化,炎症,线粒体功能,伤口愈合,脂质代谢和葡萄糖代谢。一些PPAR激动剂最近被证明可以保护阿尔茨海默病、帕金森病、亨廷顿病、肌萎缩侧索硬化症和多发性硬化症的神经元免受氧化损伤、炎症和凋亡。本文综述了PPAR激动剂在PD体内和体外模型中的神经保护作用研究进展。同样,PPAR激动剂的神经保护作用的药理学机制也进行了研究。最后,PPAR激动剂通过控制一组参与细胞存活过程的基因的表达来发挥神经保护作用,这表明它们可能是PD等致残性神经退行性疾病的潜在治疗靶点。关键词:帕金森病,神经保护,神经炎症,氧化应激,PPAR激动剂
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