Neuroprotective Effects of B-Type Cinnamon Procyanidin Oligomers on MPP+-Induced Apoptosis in a Cell Culture Model of Parkinson's Disease.
Qi XuZiyu ChenBorong ZhuYi-Ming LiManju B ReddyHuilin LiuGuodong DangQi JiaXiaojun WuPublished in: Molecules (Basel, Switzerland) (2021)
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.
Keyphrases
- induced apoptosis
- signaling pathway
- pi k akt
- reactive oxygen species
- endoplasmic reticulum stress
- water soluble
- epithelial mesenchymal transition
- cell death
- oxidative stress
- anti inflammatory
- brain injury
- cell cycle arrest
- endothelial cells
- tyrosine kinase
- risk assessment
- combination therapy
- blood brain barrier
- replacement therapy