AI Article Synopsis
- Oxidative stress contributes to neurodegenerative diseases like Parkinson's, and the antioxidant TSG from the herb Polygonum multiflorum shows potential protective effects.
- In experiments, TSG significantly improved cell viability and reduced apoptosis in rat PC12 cells affected by oxidative stress.
- The protective mechanisms of TSG involve the reduction of reactive oxygen species and nitric oxide, suggesting its potential as a therapeutic agent against oxidative stress-related neurodegenerative conditions.
Article Abstract
Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease. The molecule, 2,3,5,4'-tetrahydr- oxystilbene-2-O-β-D-glucoside (TSG), is a potent antioxidant derived from the Chinese herb, Polygonum multiflorum Thunb. In this study, we investigated the protective effect of TSG against 6-hydroxydopamine-induced apoptosis in rat adrenal pheochromocytoma PC12 cells and the possible mechanisms. Our data demonstrated that TSG significantly reversed the 6-hydroxydopamine-induced decrease in cell viability, prevented 6-hydroxydopamine-induced changes in condensed nuclei and decreased the percentage of apoptotic cells in a dose-dependent manner. In addition, TSG slowed the accumulation of intracellular reactive oxygen species and nitric oxide, counteracted the overexpression of inducible nitric oxide syntheses as well as neuronal nitric oxide syntheses, and also reduced the level of protein-bound 3-nitrotyrosine. These results demonstrate that the protective effects of TSG on rat adrenal pheochromocytoma PC12 cells are mediated, at least in part, by the ROS-NO pathway. Our results indicate that TSG may be effective in providing protection against neurodegenerative diseases associated with oxidative stress.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188584 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0026055 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
Role of PCBP2 in regulating nanovesicles loaded with curcumin to mitigate neuroferroptosis in neural damage caused by heat stroke.
J Nanobiotechnology
December 2024
Key Laboratory of Special Environmental Medicine of Xinjiang, General Hospital of Xinjiang Military Command, No. 359, Youhao North Road, Urumqi, Xinjiang, China.
Objective: This study aims to elucidate the mechanisms by which nanovesicles (NVs) transport curcumin(CUR) across the blood-brain barrier to treat hypothalamic neural damage induced by heat stroke by regulating the expression of poly(c)-binding protein 2 (PCBP2).
Methods: Initially, NVs were prepared from macrophages using a continuous extrusion method. Subsequently, CUR was loaded into NVs using sonication, yielding engineered cell membrane Nanovesicles loaded with curcumin (NVs-CUR), which were characterized and subjected to in vitro and in vivo tracking analysis.
Cytotoxic Effects of ZnO and Ag Nanoparticles Synthesized in Microalgae Extracts on PC12 Cells.
Mar Drugs
December 2024
Interdepartmental Centre of Environmental Science and Engineering (CINSA), University of Cagliari, Via San Giorgio 12, 09124 Cagliari, Italy.
The green synthesis of silver (Ag) and zinc oxide (ZnO) nanoparticles (NPs), as well as Ag/AgO/ZnO nanocomposites (NCs), using polar and apolar extracts of , offers a sustainable method for producing nanomaterials with tunable properties. The impact of the synthesis environment and the nanomaterials' characteristics on cytotoxicity was evaluated by examining reactive species production and their effects on mitochondrial bioenergetic functions. Cytotoxicity assays on PC12 cells, a cell line originated from a rat pheochromocytoma, an adrenal medulla tumor, demonstrated that Ag/AgO NPs synthesized with apolar (Ag/AgO NPs A) and polar (Ag/AgO NPs P) extracts exhibited significant cytotoxic effects, primarily driven by Ag ion release and the disruption of mitochondrial function.
View Article and Find Full Text PDFBackground: Spinal cord injury (SCI) is a neurological disease characterized by high disability and mortality rates. Tomatidine, a natural steroid alkaloid, has been evidenced to have neuroprotective properties. However, the underlying mechanisms of tomatidine in treating SCI remain ambiguous.
View Article and Find Full Text PDFDental Pulp Regeneration in Dogs Using a CCR3 Antagonist Without Transplantation of Dental Pulp Stem Cells.
J Endod
December 2024
Tokyo New Drug Research Laboratories, Pharmaceutical Business Unit, Kowa Company, Ltd., 2-17-43 Noguchi-cho, Higashimurayama, Tokyo, Japan.
Introduction: Our previous study showed that transplantation of dental pulp stem cells (DPSCs) in combination with a chemokine receptor 3 (CCR3) antagonist into the root canals of aged dogs promoted dental pulp regeneration. In this study, we attempted to regenerate dental pulp in young dogs using a CCR3 antagonist without DPSC transplantation.
Methods: The teeth of dogs were histologically evaluated 4 weeks after extraction of the pulp and administration of scaffold materials and CCR3 antagonist (KDH-136) into the root canal.
Microcystin-LR induces neuronal damage through mitophagy defects resulted from the downregulated transcription of Scd2 by directly targeting IGF-1R.
Environ Pollut
December 2024
Department of Environmental Hygiene, College of Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing 400038, The People's Republic of China. Electronic address:
Microcystin-LR (MC-LR), a prevalent cyanotoxin present in hazardous cyanobacterial blooms, is recognized as a neurotoxic environmental pollutant that induces brain damage and neurobehavioral deficits. However, the mechanisms underlying MC-LR-induced neurotoxicity remain unclear. This study aims to elucidate the role of mitophagy in MC-LR-induced neurotoxicity both in vitro and in vivo.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!