Gastrodia elata Blume alleviates L-DOPA-induced dyskinesia by normalizing FosB and ERK activation in a 6-OHDA-lesioned Parkinson’s disease mouse model
- Equal contributors
1 Studies of Translational Acupuncture Research (STAR), Acupuncture & Meridian Science Research Center (AMSRC), Kyung Hee University, 1 Hoegi-dong, Dongdaemoon-gu, Seoul 130-701, Republic of Korea
2 Department of Pharmacy, College of Pharmacy, Hanyang University, Ansan-si, Gyeonggi-do 426-791, Republic of Korea
3 Dongguk University Research Institute of Biotechnology, Dongguk University, 3-26, Pil Dong, Choong-Gu, Seoul 100-715, Republic of Korea
4 Department of Neurology and Cardiology of Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul 134-727, Republic of Korea
5 Stroke and Neurological Disorders Center, Kyung Hee University Hospital at Gangdong, 149 Sangil-dong, Gangdong-gu, Seoul 134-727, Republic of Korea
BMC Complementary and Alternative Medicine 2014, 14:107 doi:10.1186/1472-6882-14-107Published: 20 March 2014
Gastrodia elata Blume (GEB), commonly used medicinal herb, has been reported as a promising candidate for neurodegenerative diseases such as Parkinson’s disease. The dopamine precursor, L-3,4-dihydroxyphenylalanine (L-DOPA), is the gold-standard drug for Parkinson’s disease, but long-term treatment results in the L-dopa-induced dyskinesia (LID). This study was undertaken to examine the beneficial effects of GEB on L-DOPA induced dyskinesia in 6-hydroxydopamine (6-OHDA)-induced experimental Parkinsonism.
We tested the effects of GEB on LID in 6-hydroxydopamine hydrochloride-hemiparkinsonian mice. To analyze the dyskinetic anomalies, we measured abnormal involuntary movement (AIM). Immunohistological analyses of pERK and FosB expressions in the striatum are performed to explore the mechanism of GEB on LID.
The finding of this study demonstrated that GEB (200, 400 and 800 mg/kg) alleviated L-dopa induced AIMs in a dose-dependent manner. In each integrative AIM subtype analysis, we also found that the GEB (400 and 800 mg/kg) treatment decreased L-DOPA-induced axial, limb, orolingual, and locomotive AIMs compared to the LID group. In addition, GEB normalized the abnormal LID-induced increase of pERK1/2 and FosB, the immediate early genes of LID in the striatum.
In conclusion, our results provide a novel insight into the pharmacological actions of GEB that could have a benefit for PD patients through the reduction of LID.