This focus of our research is to investigate the protective effect of Baicalin on apoptosis and mTOR/AKT/GSK-3β pathway in substantia nigra neurons in a rat model for Parkinson's disease, induced by 6-Hydroxydopamine. Thirty healthy female Sprague-Dawley rats were randomly divided into control group, model group, and Baicalin group. The Parkinson model was established by injecting 6-Hydroxydopamine into the right substantia nigra of rats in model and Baicalin group. The rats in Baicalin group were intragastrically administered with Baicalin (25 mg/kg/day) for four weeks. At the same time, the rats in control and model groups were intragastrically administered with equivalent solvents. We observed the rat turns, rotation speed and left forelimb usage. The protein expression levels of α-SYN, mTOR, AKT, and GSK-3β in substantia nigra were detected by immunohistochemistry and Western blotting. Compared with model group, Baicalin significantly reduced the number of rotation speeds and neuron apoptosis (P < 0.001, respectively). However, the left forelimb use rate was notably increased after treatment with Baicalin (P < 0.001, respectively). Also, Baicalin decreased the expression levels of α-SYN, mTOR, AKT, and GSK-3β in rats when compared with those in model group (P < 0.001, respectively).
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http://dx.doi.org/10.31083/j.jin.2019.04.192 | DOI Listing |
Arch Gerontol Geriatr
December 2024
Department of Neurology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200065, China. Electronic address:
Mol Cell Biochem
January 2025
Neurodegenerative Diseases Laboratory, Center for Biomedicine, Universidad Mayor, Avenida Alemania 0281, 4780000, Temuco, La Araucanía, Chile.
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by tremor, rigidity, and bradykinesia, beginning with early loss of dopaminergic neurons in the ventrolateral substantia nigra and advancing to broader neurodegeneration in the midbrain. The clinical heterogeneity of PD and the lack of specific diagnostic tests present significant challenges, highlighting the need for reliable biomarkers for early diagnosis. Alpha-synuclein (α-Syn), a protein aggregating into Lewy bodies and neurites in PD patients, has emerged as a key biomarker due to its central role in PD pathophysiology and potential to reflect pathological processes.
View Article and Find Full Text PDFEur J Neurol
January 2025
Institut du Cerveau-Paris Brain Institute ICM, Sorbonne Université, Inserm 1127, CNRS 7225, Hôpital de la Pitié Salpêtrière Paris, Paris, France.
Objective: Spinocerebellar ataxias (SCA) are neurodegenerative diseases with widespread lesions across the central nervous system. Ataxia and spasticity are usually predominant, but patients may also present with parkinsonism. We aimed to characterize substantia nigra pars compacta (SNc) degeneration in SCA2 and 7 using neuromelanin-sensitive imaging.
View Article and Find Full Text PDFNeurosci Bull
January 2025
Center for Translational Neuromedicine and Neurology, School of Life Sciences, Institute for Brain Sciences Research, Henan University, Huaihe Hospital of Henan University, Kaifeng, 475004, China.
Parkinson's disease (PD), a chronic and common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the dense part of the substantia nigra and abnormal aggregation of alpha-synuclein. Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic insulin resistance and deficiency in insulin secretion. Extensive evidence has confirmed shared pathogenic mechanisms underlying PD and T2DM, such as oxidative stress caused by insulin resistance, mitochondrial dysfunction, inflammation, and disorders of energy metabolism.
View Article and Find Full Text PDFNPJ Parkinsons Dis
January 2025
Department of Neuroscience & Experimental Therapeutics, Texas A&M University College of Medicine, 8447 John Sharp Pkwy, Bryan, TX, 77807-3260, USA.
The smoking cessation drug cytisine exerts neuroprotection in substantia nigra pars compacta (SNc) dopaminergic (DA) neurons of female but not male 6-hydroxydopamine (6-OHDA) lesioned parkinsonian mice. To address the important question of whether circulating 17β-estradiol mediates this effect, we employ two mouse models aimed at depleting systemically circulating 17β-estradiol: (i) bilateral ovariectomy (OVX), and (ii) aromatase inhibition with systemically administered letrozole. In both models, depleting systemically circulating 17β-estradiol in female 6-OHDA lesioned parkinsonian mice results in the loss of cytisine-mediated neuroprotection as measured using apomorphine-induced contralateral rotations and SNc DA neurodegeneration.
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