Neuroprotective Effects of B-Type Cinnamon Procyanidin Oligomers on MPP<sup>+</sup>-Induced Apoptosis in a Cell Culture Model of Parkinson’s Disease
Qi Xu,
Ziyu Chen,
Borong Zhu,
Yiming Li,
Manju B. Reddy,
Huilin Liu,
Guodong Dang,
Qi Jia,
Xiaojun Wu
Affiliations
Qi Xu
School of Public Health, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Ziyu Chen
Shanghai Key Laboratory of Compound Chinese Medicine, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Borong Zhu
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Yiming Li
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Manju B. Reddy
Department of Food Science and Human Nutrition, Iowa State University, Ames, IA 50010, USA
Huilin Liu
School of Public Health, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Guodong Dang
School of Public Health, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Qi Jia
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
Xiaojun Wu
Shanghai Key Laboratory of Compound Chinese Medicine, The Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
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.
