Background: Parkinson's disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. The purpose of this study was to examine neuroprotective effects of Hepad S1, an herbal medicine used for the treatment of PD, in and models of PD.
Methods: Differentiated neuronal PC12 cells underwent a cytotoxicity assay and oxidative stress analysis including DCF-DA staining, glutathione, and malondialdehyde, after exposure to 1-methyl-4-phenylpyridium (MPP+). Male Sprague-Dawley rats were used as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD models. After 4-week oral administration of Hepad S1 (200, 300, 400, and 500 mg/kg/day), the levels of complex enzyme I activity and dopamine, and dopaminergic neuronal cell number in substantia nigra were measured by enzyme linked immune-sorbent assay (ELISA) and microscopic observation, respectively. Circulating serotonin and orexin A were also examined by ELISA.
Results: Hepad S1 pretreatment prevented the ability of MPP+ challenge to decrease glutathione and increase lipid peroxidation in cells, indicating antioxidant activity. Hepad S1 recovered MPTP-induced decreases in complex I enzyme activity and enhanced dopamine availability in substantia nigra. Serum levels of serotonin and orexin A were increased by Hepad S1 treatment in model animals. Hepad S1 treatment was associated with the preservation of tyrosine hydroxylase-positive cells in the substantia nigra of MPTP-treated rats.
Conclusions: Hepad S1 exerts antioxidant and neuroprotective effects on neurons of the substantia nigra in a rodent model of PD.
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http://dx.doi.org/10.1016/j.imr.2019.07.005 | DOI Listing |
J Integr Neurosci
December 2024
Federal State Budgetary Educational Institution, Institute of Theoretical and Experimental Biophysics, 142290 Pushchino, Russia.
Background: Long-term use of levodopa, a metabolic precursor of dopamine (DA) for alleviation of motor symptoms in Parkinson's disease (PD), can cause a serious side effect known as levodopa-induced dyskinesia (LID). With the development of LID, high-frequency gamma oscillations (~100 Hz) are registered in the motor cortex (MCx) in patients with PD and rats with experimental PD. Studying alterations in the activity within major components of motor networks during transition from levodopa-off state to dyskinesia can provide useful information about their contribution to the development of abnormal gamma oscillations and LID.
View Article and Find Full Text PDFNMR Biomed
February 2025
Department of Radiology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China.
Asymmetry is a natural characteristic of Parkinson's disease (PD), which can be used to distinguish PD from atypical parkinsonism. Chemical exchange saturation transfer (CEST) has demonstrated value in reflecting the subtle changes related to neuron loss and abnormal protein accumulation in PD but has not been used to investigate asymmetry in PD. This study aimed to examine asymmetrical changes in the mesencephalic nucleus of PD patients with motor asymmetry using four-pool CEST analysis and to explore the relationship between imaging asymmetry and motor asymmetry.
View Article and Find Full Text PDFTransl Neurodegener
December 2024
Department of Anatomy and Medical Imaging, University of Auckland, 85 Park Road, Grafton, , Auckland, 1142, New Zealand.
Background: Parkinson's disease (PD) and multiple system atrophy (MSA) are classified as α-synucleinopathies and are primarily differentiated by their clinical phenotypes. Delineating these diseases based on their specific α-synuclein (α-Syn) proteoform pathologies is crucial for accurate antemortem biomarker diagnosis. Newly identified α-Syn pathologies in PD raise questions about whether MSA exhibits a similar diversity.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
December 2024
Anhui Provincial Center for Neural Regeneration Technology and New Medical Materials Engineering Research, Bengbu Medical University, Bengbu 233000, China.
Objectives: To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD).
Methods: Wild-type (WT) male C57BL/6 mice and Parkin mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting.
Int Immunopharmacol
December 2024
Laboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China. Electronic address:
Astrocyte-mediated neuroinflammation plays a key role in Parkinson's disease (PD) progression. The proinflammatory protein S100A9 is linked to various neurodegenerative diseases, but its involvement in astrocyte activation in PD remains unclear. Here, we investigate the role of S100A9 in astrocyte-mediated neuroinflammation in PD.
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