Background: Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive death of dopaminergic neurons in the substantia nigra pars compacta (SNpc).
Aims: To study if tenuigenin (TEN), the main active component of Polygala tenuifolia, can protect dopaminergic neurons from inflammation-mediated damage in vivo.
Methods: We observed the effects of TEN on lipopolysaccharide (LPS) induced PD model by behavioral analysis, high-performance liquid chromatography, immunohistochemistry and enzyme-linked immunoadsorbent assay, etc.
Results: We showed that a single intranigral dose of LPSs (10 μg) induced microglial activation, reduced the survival ratio of tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the SNpc and reduced dopamine (DA) content in the striatum. Treatment with 300 mg/kg TEN once per day over 14 weeks improved the survival rate of TH-ir neurons in the SNpc to 75%, on the non-injected side. Treatment with 200 or 300 mg/kg TEN once per day over 14 weeks significantly improved DA levels in the striatum to 73% and 81% on the non-injected side, respectively. The excessive production of cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, was abolished by TEN administration.
Conclusion: Our results suggest that TEN may play a role in protecting dopaminergic neurons against inflammatory challenge.
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http://dx.doi.org/10.1111/j.1755-5949.2012.00347.x | DOI Listing |
Inflammation
January 2025
Department of Chemistry, University of Agriculture Faisalabad, Faisalabad, Pakistan.
Parkinson's disease (PD) stands as the sec most prevalent incapacitating neurodegenerative disorder characterized by deterioration of dopamine-producing neurons in the substantia nigra. Coenzyme Q10 (CoQ10) has garnered attention as a potential antioxidant, anti-inflammatory agent and enhancer of mitochondrial complex-I activity. This study aimed to examine and compare the effectiveness of liposomal and non-encapsulated CoQ10 in rotenone induced-PD mouse model over a 21-day treatment duration.
View Article and Find Full Text PDFNeurosci Lett
January 2025
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico. Electronic address:
Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to significant motor and non-motor symptoms. Beta oscillations in cortical areas are a pathognomonic sign. Here we ask whether these oscillations can be recorded in in vitro cortical tissue despite severing the cortico-basal ganglia-thalamo-cortical loop.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Physiology, School of Medicine, and Co-innovation Center of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong 226001 China. Electronic address:
Parkinson' s disease (PD) is a chronic neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra (SN). Our research has demonstrated that the levels of interleukin (IL)-17A are elevated in the SN of rodent models of PD, and that IL-17A accelerates neurodegeneration in PD depending on microglial activation. Furthermore, existing studies indicate that exosomes released by activated microglia may play a significant role as mediators of neurodegeneration in PD.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, China.
The main characteristics of Parkinson's disease (PD) are the loss of dopaminergic (DA) neurons and abnormal aggregation of cytosolic proteins. However, the exact pathogenesis of PD remains unclear, with ferroptosis emerging as one of the key factors driven by iron accumulation and lipid peroxidation. Glial cells, including microglia, astrocytes, and oligodendrocytes, serve as supportive cells in the central nervous system (CNS), but their abnormal activation can lead to DA neuron death and ferroptosis.
View Article and Find Full Text PDFGene networks encapsulate biological knowledge, often linked to polygenic diseases. While model system experiments generate many plausible gene networks, validating their role in human phenotypes requires evidence from human genetics. Rare variants provide the most straightforward path for such validation.
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