Autophagy-related protein expression in the substantia nigra and eldepryl intervention in rat models of Parkinson's disease.
Autophagy has been shown to participate in the pathogenesis of Parkinson's disease (PD), but its precise mechanism remains poorly understood. This study observed autophagy, autophagy-related protein Beclin1 and microtubule-associated protein 1 light chain 3 (LC3) expression in substantia nigra, and eldepryl effects on their expression, as well as explored autophagy effects on the onset of PD and the mechanism of action of eldepryl on PD in rat models. Models of PD were established by subcutaneous injection of rotenone through back of the neck. Results indicated that Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher in substantia nigra of rats in the model group compared with the control group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher at 8 days than that at 4 days in the model group, showing significant differences. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower in the rat substantia nigra of the eldepryl group than in the model group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower at 8 days than at 4 days in the eldepryl group, showing significant differences. Results suggested that autophagy plays a key role in the onset of PD. Eldepryl exerts therapeutic effects on PD by inhibiting autophagy of nerve cells in substantia nigra of rat models of PD.
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China. Electronic address: liubintsh68@126.com.
Bin
B
Liu
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Jing
J
Sun
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Jinxia
J
Zhang
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Wenjing
W
Mao
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Yuanyuan
Y
Ma
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Shiying
S
Li
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Xiaohua
X
Cheng
First Department of Neurology, Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, Hebei Province, China.
Chaonan
C
Lv
D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D000071186:Beclin-1; D004195:Disease Models, Animal; D007306:Insecticides / Q000633:toxicity; D008297:Male; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012402:Rotenone / Q000633:toxicity; D012642:Selegiline / Q000627:therapeutic use*; D013378:Substantia Nigra / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D013997:Time Factors
D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; D007306:Insecticides; D008869:Microtubule-Associated Proteins; D018696:Neuroprotective Agents; D012402:Rotenone; D012642:Selegiline; C512829:Becn1 protein, rat; C526109:Anxa3 protein, rat
Autophagy; Beclin1; Eldepryl; LC3; Parkinson׳s disease; Substantia nigra