Neuroprotective Effect of the n-Hexane Extracts of Laurus nobilis L. in Models of Parkinson’s DiseaseNeuroprotective Effect of the n-Hexane Extracts of Laurus nobilis L. in Models of Parkinson’s Disease
- Other Titles
- Neuroprotective Effect of the n-Hexane Extracts of Laurus nobilis L. in Models of Parkinson’s Disease
- Authors
- Ahrom Ham; 신종헌; 오기봉; 이성진; 남궁우; Uk Koo; 김경호; 마응천
- Issue Date
- 2011
- Publisher
- 한국응용약물학회
- Keywords
- Laurus nobilis L; Dopamine; Parkinson’s disease; Neuroprotective; α-synuclein
- Citation
- Biomolecules & Therapeutics, v.19, no.1, pp.118 - 125
- Journal Title
- Biomolecules & Therapeutics
- Volume
- 19
- Number
- 1
- Start Page
- 118
- End Page
- 125
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/17353
- ISSN
- 1976-9148
- Abstract
- Free radical scavenging and antioxidants have attracted attention as a way to prevent the progression of Parkinson’s disease (PD). This study was carried out to investigate the effects of n-hexane fraction from Laurus nobilis L. (Lauraceae) leaves (HFL) on dopamine (DA)-induced intracellular reactive oxygen species (ROS) production and apoptosis in human neuroblastoma SH-SY5Y cells. Compared with apomorphine (APO, IC_(50)=18.1 μM) as a positive control, the HFL IC_(50) value for DA-induced apoptosis was 3.0 μg/ml, and two major compounds from HFL, costunolide and dehydrocostus lactone, were 7.3 μM and 3.6 μM, respectively.
HFL and these major compounds signifi cantly inhibited ROS generation in DA-induced SH-SY5Y cells. A rodent 6-hydroxydopamine (6-OHDA) model of PD was employed to investigate the potential neuroprotective effects of HFL in vivo. 6-OHDA was injected into the substantia nigra of young adult rats and an immunohistochemical analysis was conducted to quantitate the tyrosine hydroxylase (TH)-positive neurons. HFL signifi cantly inhibited 6-OHDA-induced TH-positive cell loss in the substantia nigra and also reduced DA induced α-synuclein (SYN) formation in SH-SY5Y cells. These results indicate that HFL may have neuroprotective effects against DA-induced in vitro and in vivo models of PD.
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