Phytic acid attenuates inflammatory responses and the levels of NF-κB and p-ERK in MPTP-induced Parkinson's disease model of mice.
Phytic acid (PA) is a naturally occurring constituent which exhibits protective action in Parkinson's disease (PD). Inflammation in the central nervous system (CNS) is strongly associated with neuronal death in PD. However, the molecular mechanism of the protective effect of PA in PD has not been fully elucidated. In this study, we tried to testify the protection of PA on neuron and inflammatory responses in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model of mice and investigated the mechanism involved in them. Motor behavior test and tyrosine hydroxylase (TH) immunohistochemistry method showed PA significantly inhibited MPTP-induced dopaminergic cell loss in the substantia nigra (SN). Moreover, using immunohistochemistry method and quantitative polymerase chain reaction (qPCR), microglial activation and inducible nitric oxide synthase (iNOS) were found to be markedly repressed by PA. Via western blot assay, expressions of nuclear factor κB (NF-κB) and phosphorylated extracellular signal-regulated kinase (p-ERK) were significantly attenuated by PA. In conclusion, it is suggested that PA has a neuroprotective effect in MPTP-induced PD model and the neuroprotection is correlated with its anti-inflammatory effect which may be associated with suppression of pathways that involved in NF-κB and p-ERK.
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Yuqiang
Y
Lv
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China. Electronic address: qyzhang_zheng@126.com.
Zheng
Z
Zhang
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China. Electronic address: qingyi001@126.com.
Lin
L
Hou
Department of Pharmacology, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Li
L
Zhang
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Jinyu
J
Zhang
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Yuehua
Y
Wang
The Third People's Hospital of Qingdao, Qingdao University, Qingdao, Shandong 266041, China.
Cun
C
Liu
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Pingping
P
Xu
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Lu
L
Liu
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Xiaoying
X
Gai
Department of Biochemistry, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College, Qingdao University, Qingdao, Shandong 266021, China.
Tingxiu
T
Lu
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002135:Calcium-Binding Proteins / Q000378:metabolism; D059290:Dopaminergic Neurons / Q000473:pathology; D004789:Enzyme Activation; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D008840:Microfilament Proteins / Q000378:metabolism; D017628:Microglia / Q000378:metabolism; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D009048:Motor Skills / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010300:Parkinson Disease / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D065842:Pars Compacta / Q000187:drug effects / Q000473:pathology; D010766:Phosphorylation; D010833:Phytic Acid / Q000494:pharmacology* / Q000627:therapeutic use
C491049:Aif1 protein, mouse; D000893:Anti-Inflammatory Agents; D002135:Calcium-Binding Proteins; D008840:Microfilament Proteins; D016328:NF-kappa B; D018696:Neuroprotective Agents; D010833:Phytic Acid; D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D052247:Nitric Oxide Synthase Type II; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3
ERK; Inflammation; NF-κB; Parkinson’s disease; Phytic acid; iNOS