title: β-asarone and levodopa co-administration protects against 6-hydroxydopamine-induced damage in parkinsonian rat mesencephalon by regulating autophagy: down-expression Beclin-1 and light chain 3B and up-expression P62.
abstract: In this study, we investigated Beclin-1, light chain (LC)3B, and p62 expression in 6-hydroxydopamine (6-OHDA)-induced parkinsonian rats after β-asarone and levodopa (l-dopa) co-administration. Unilateral 6-OHDA injection into the medial forebrain bundle was used to create the models, except in sham-operated rats. Rats were divided into eight groups: sham-operated group; 6-OHDA model group; madopar group (75 mg/kg, per os (p.o.)); l-dopa group (60 mg/kg, p.o.); β-asarone group (15 mg/kg, p.o.); β-asarone + l-dopa co-administered group (15 mg/kg + 60 mg/kg, p.o.); 3-methyladenine group (500 nmol, intraperitoneal injection); and rapamycin group (1 mg/kg, intraperitoneal injection). Then, Beclin-1, LC3B, and p62 expression in the mesencephalon were detected. The mesencephalon was also observed by transmission electron microscope. The results showed that Beclin-1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l-dopa, β-asarone, and co-administered groups when compared with the 6-OHDA model. Beclin-1 and LC3B expression in the β-asarone and co-administered groups were less than in the madopar or l-dopa groups, whereas p62 expression in the β-asarone and co-administered groups was higher than in the madopar or l-dopa groups. In addition, a significant decrease in autophagosome was exhibited in the β-asarone and co-administered groups when compared with the 6-OHDA group. Our findings indicate that Beclin-1 and LC3B expression decreased, whereas p62 expression increased after co-administration treatment. In sum, all data suggest that the co-administration of β-asarone and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity.
authors.affiliation: Experimental Center, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Huang
authors.forename: Min-Zhen
authors.initials: MZ
authors.lastname: Deng
authors.forename: Yu-Ping
authors.initials: YP
authors.lastname: He
authors.forename: Yong-Qi
authors.initials: YQ
authors.lastname: Fang
mesh_terms: D000081248:Allylbenzene Derivatives; D000818:Animals; D000840:Anisoles / Q000008:administration & dosage / Q000494:pharmacology*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D001343:Autophagy / Q000187:drug effects*; D000071186:Beclin-1; D059290:Dopaminergic Neurons / Q000187:drug effects / Q000473:pathology; D015536:Down-Regulation / Q000187:drug effects; D004347:Drug Interactions; D005260:Female; D007980:Levodopa / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D008636:Mesencephalon / Q000378:metabolism / Q000473:pathology*; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D016627:Oxidopamine / Q000009:adverse effects*; D010300:Parkinson Disease / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D051758:Transcription Factor TFIIH; D014157:Transcription Factors / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000081248:Allylbenzene Derivatives; D000840:Anisoles; D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C115010:Becn1 protein, mouse; C490981:Gtf2h1 protein, mouse; C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D014157:Transcription Factors; C012195:asarone; D051758:Transcription Factor TFIIH; D007980:Levodopa; D016627:Oxidopamine
keywords: Beclin-1; autophagy; levodopa; light chain 3B; p62; β-asarone