Neuroprotective Effects of [beta]-Asarone Against 6-Hydroxy Dopamine-Induced Parkinsonism via JNK/Bcl-2/Beclin-1 Pathway

• Published in: Molecular neurobiology Vol. 53; no. 1; p. 83
• Main Authors: Zhang, Sheng, Gui, Xue-hong, Huang, Li-ping, Deng, Min-zhen, Fang, Ruo-ming, Ke, Xue-hong, He, Yu-ping, Li, Ling, Fang, Yong-qi
• Format: Journal Article
• Language: English
• Published: Totowa Springer Nature B.V 01.01.2016
• Subjects: Autophagy; Dopamine; Neurobiology; Neurodegeneration; Parkinson's disease
• ISSN: 0893-7648; 1559-1182
• DOI: 10.1007/s12035-014-8950-z

[beta]-asarone, a major component of Acorus tatarinowii Schott, has positive effects in neurodegeneration disease, however, its effect on the Parkinson's disease (PD) remains unclear. In this study, the effects of [beta]-asarone on behavioral tests, neurotransmitters, tyrosine hydroxylase (TH), and [alpha]-synuclein ([alpha]-syn) were investigated in 6-hydroxydopamine (6-OHDA) induced rats. Furthermore, the JNK/Bcl-2/Beclin-1 autophagy pathway was also studied. The results showed that [beta]-asarone improved the behavioral symptoms of rats in the open field, rotarod test, initiation time, and stepping time. And it increased the HVA, Dopacl, and 5-HIAA levels in striatum but not the DA and 5-HT levels. After administration of [beta]-asarone, the TH level was elevated but the [alpha]-syn was declined in rats. It inhibited the expressions of LC3-II, but increased the p62 expression in SN4741 cells. Moreover, it affected the expressions of Beclin-1, Bcl-2, JNK, and p-JNK in vivo. We deduced that [beta]-asarone may firstly downregulate expressions of JNK and p-JNK, and then indirectly increase the expression of Bcl-2. And the function of Beclin-1 could be inhibited, which could inhibit autophagy activation. Collectively, all data indicated that [beta]-asarone may be explored as a potential therapeutic agent in PD therapy.