Puerarin prevents inflammation and apoptosis in the neurocytes of a murine Parkinson's disease model.
The aim of this study was to investigate Parkinson's disease (PD) using a murine model of PD. Specifically, we aimed to explore the mechanism by which puerarin prevents inflammation and apoptosis in neurocytes. Eighty healthy male C57/BL6 mice were randomly selected and divided into four groups (N = 20 each): control group; PD group; PD+puerarin group; and puerarin group. At the end of the treatment period, the animals' brains were removed after perfusion and decollation. The protein expression levels of tyrosine hydroxylase (TH) in the murine brains were assessed by immunohistochemistry and the protein expression levels of TH, glial fibrillary acidic protein (GFAP), inducible nitric oxide synthase (iNOS), cleaved Caspase-3, and Bax in the substantia nigra and corpus striatum of the animals were assessed by western blotting. The spontaneous activity of the PD mice was found to be significantly higher after puerarin treatment and the distance traveled by mice in an open field assessment was 1700 cm further in puerarin-treated PD mice than in PD mice. Immunohistochemistry and western blotting analyses indicated that the expression of TH was significantly higher (2.63-fold) in puerarin-treated PD mice than in untreated PD mice and that the expression of GFAP in PD mice was significantly reduced (~45%) by puerarin treatment. These findings lead us to conclude that puerarin significantly alleviates 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine-induced injury in dopaminergic neurons. Puerarin mediates anti-apoptotic and anti-inflammatory activities and plays a neuroprotective role.
Department of Neurology, General PLA Hospital, Beijing, China.|Department of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
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M
Jiang
Department of Neurology, the People's Hospital, Hohhot, Inner Mongolia, China.
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Q
Yun
Department of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
G
G
Niu
Department of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Y
Y
Gao
Department of Neurology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
F
F
Shi
Department of Neurology, General PLA Hospital, Beijing, China shengyuanyu_bj@163.com.
S
S
Yu
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control*; D007529:Isoflavones / Q000494:pharmacology* / Q000627:therapeutic use*; D008297:Male; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010300:Parkinson Disease / Q000188:drug therapy* / Q000473:pathology*; D013378:Substantia Nigra / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D005904:Glial Fibrillary Acidic Protein; D007529:Isoflavones; D051028:bcl-2-Associated X Protein; D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D052247:Nitric Oxide Synthase Type II; D014446:Tyrosine 3-Monooxygenase; D053148:Caspase 3; C033607:puerarin