Abstract
Cinnamon procyanidin oligomers (CPOs) are water-soluble components extracted from cinnamon. This study aims to explore the neuroprotection of B-type CPO (CPO-B) against 1-methyl-4-phenylpyridinium (MPP+)-mediated cytotoxicity and the molecular mechanisms underlying its protection. The results demonstrated that CPO-B showed protection by increasing cell viability, attenuating an intracellular level of reactive oxygen species, downregulating cleaved caspase-3 expression, and upregulating the Bcl-2/Bax ratio. Moreover, CPO-B completely blocked the dephosphorylation of extracellular, signal-regulated kinase 1 and 2 (Erk1/2) caused by MPP+. Treatment with an Erk1/2 inhibitor, SCH772984, significantly abolished the neuroprotection of CPO-B against MPP+. Taken together, we demonstrate that CPO-B from cinnamon bark provided protection against MPP+ in cultured SH-SY5Y cells, and the potential mechanisms may be attributed to its ability to modulate the dysregulation between pro-apoptotic and anti-apoptotic proteins through the Erk1/2 signaling pathway. Our findings suggest that the addition of cinnamon to food or supplements might benefit patients with PD.
Highlights
Parkinson’s disease (PD) is a devastating and irreversible degenerative disorder that afflicts about 1.5% of the population aged 65 years and over in the world [1]
This study aims to assess whether Cinnamon procyanidin oligomers (CPOs)-B attenuates MPP+-induced cytotoxicity in the dopaminergic cell SH-SY5Y, a cell model of PD, and to explore whether it exerts neuroprotection through activating the Erk1/2 signaling pathway and modulating the dysregulation between pro-apoptotic and anti-apoptotic proteins
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Summary
Parkinson’s disease (PD) is a devastating and irreversible degenerative disorder that afflicts about 1.5% of the population aged 65 years and over in the world [1]. Mitogen-activated protein kinases (MAPKs) are a type of serine/threonine protein kinases, consisting of extracellular, signal-regulated kinase (Erk) 1 and 2 (Erk1/2), P38 isoforms, and c-Jun Nterminal kinase (JNK) [2]. They are essential components of the signaling network and function as an integral part in cellular processes, such as growth, differentiation, apoptosis, survival, and proliferation [3]. The exact mechanisms responsible for neuronal death in PD remain unclear, research suggests that abnormal regulation of MAPKs may contribute to the pathogenesis of PD by triggering the dysregulation of pro-apoptotic and anti-apoptotic pathways, inducing neuroinflammation, oxidative stress, and mitochondrial dysfunction [4,5]. MAPK signaling pathways are considered as a possible therapeutic solution to PD treatment
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