Abstract
Humulus japonicus is an annual plant belonging to the Cannabacea family, and it has been traditionally used to treat pulmonary tuberculosis, dysentery, chronic colitis, and hypertension. We investigated the active components against Parkinson’s disease from H. japonicus fraction (HJF) using high performance liquid chromatography (HPLC) coupled with quadruple-time-of-flight mass spectroscopy (qTOF-MS) and NMR. Fourteen compounds were isolated from HJF, including one new compound, using HPLC-qTOF-MS and NMR. The major compounds of HJF were luteolin-7-O-glucoside and apigenin-7-O-glucoside, and there was approximately 12.57- and 9.68-folds increase in the contents of these flavonoids compared to those of the 70% EtOH extract. Apigenin and luteolin exhibited the strongest inhibitory effects on monoamine oxidase (MAO) B enzyme activity. In animal studies, limb-use behavior was significantly reduced by unilateral 6-OHDA lesion and ipsilateral rotations. These results indicated that oral administration of 300 mg/kg HJF resulted in the improvement of motor asymmetry and motor impairment in unilateral 6-OHDA-lesioned mice. HJF, including active components leads to an improvement of motor behavior in a Parkinson’s disease mouse model.
Highlights
Parkinson’s disease (PD) is a common neurodegenerative disorder that caused motor problems such as resting tremor, muscle rigidity, and postural instability [1]
These results indicate that oral administration of 300 mg/kg H. japonicus fraction (HJF) leads to improved motor asymmetry and motor impairment in unilateral 6-OHDA-lesioned mice
The right forelimb damaged by unilateral 6-OHDA injection was effectively improved, and the rotations under the presynaptically active d-AMPH were markedly suppressed by the administration of 300 mg/kg HJF
Summary
Parkinson’s disease (PD) is a common neurodegenerative disorder that caused motor problems such as resting tremor, muscle rigidity, and postural instability [1]. PD pathogenesis is associated with genetic disposition, age and environmental factors, mitochondrial dysfunction, oxidative damage, inflammation, and microgliosis [2,3]. Oxidative damage by the generation of reactive oxygen species (ROS) causes neuronal membrane damage, including damage to membrane proteins, unsaturated lipids, and DNA [4]. Recent studies have suggested that the side chains of membrane proteins and lipids are modified by ROS, and a reduction in membrane unsaturation is associated with decreased membrane. The brain is susceptible to oxidative stress damage due to the high concentration of polyunsaturated fatty acids and oxygen. Oxidative damage by 6-hydroxydopamine (6-OHDA) induces apoptosis in various neurons [6], and toxicity and apoptosis by 6-OHDA are induced by activation of the mitogen-activated protein kinase (MAPK)
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