scholarly journals Inhibitory Effects Induced by Vicia faba, Uncaria rhyncophylla, and Glycyrrhiza glabra Water Extracts on Oxidative Stress Biomarkers and Dopamine Turnover in HypoE22 Cells and Isolated Rat Striatum Challenged with 6-Hydroxydopamine

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 602 ◽  
Author(s):  
Giustino Orlando ◽  
Annalisa Chiavaroli ◽  
Sheila Leone ◽  
Luigi Brunetti ◽  
Matteo Politi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vicia Faba ◽  
Glycyrrhiza Glabra ◽  
Rat Striatum ◽  
Protective Effects ◽  
Related Disorder ◽  
Water Extracts ◽  
6 Hydroxydopamine ◽  
Pharmacological Association ◽  
Isolated Rat

Background: Parkinson’s disease (PD) is the most common and progressive neurodegenerative and oxidative stress-related disorder, characterized by a dramatic loss of dopamine (DA) neurons in the nigrostriatal tissue. The first-line drug for PD treatment is represented by l-dopa, although clinical and preclinical studies pointed out the potential efficacy of medicinal plant- and food-derived antioxidants as brain protective agents. In this regard, the potential application of Vicia faba, Uncaria rhyncophylla, and Glycyrrhiza glabra extracts is of noteworthy interest, despite a lack of information in the scientific literature as regards their effect on striatal DA level. Methods: The protective effects of V. faba, U. rhyncophylla, and G. glabra water extracts were investigated on HypoE22 cells and isolated rat striatum specimens challenged with 6-hydroxydopamine (6-OH-DA). The extract effects against lactate dehydrogenase (LDH), nitrites, and 8-iso-prostaglandin(PG)F2α were evaluated using either single-extract treatments or a treatment with a pharmacological association. Additionally, the turnover of DA was measured. Results: The pharmacological association of the extracts was the most effective in contrasting the upregulated LDH and nitrite levels and in reducing striatal DA turnover. Conclusion: The present findings corroborate the rational for the traditional use of V. faba, G. glabra, and U. rhyncophylla extracts, supporting their pharmacological association in order to improve their protective effects.

scholarly journals Protective Effects of Saponin Mixture, Isolated from <i>Astragalus monspessulanus</i> subsp. <i>monspessulanus</i> on Tert-Butyl Hydroperoxide—Induced Oxidative Stress in Isolated Rat Hepatocytes

2015 ◽  
Vol 06 (06) ◽  
pp. 799-803 ◽  
Author(s):  
Magdalena Spasova Kondeva-Burdina ◽  
Viktor Bratkov ◽  
Rumyana Lubomirova Simeonova ◽  
Vessela Bisserova Vitcheva ◽  
Ilina Nikolaeva Krasteva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Rat Hepatocytes ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide ◽  
Isolated Rat

The protective effects of melanoidins in adriamycin-induced oxidative stress in isolated rat hepatocytes

2004 ◽  
Vol 84 (13) ◽  
pp. 1701-1707 ◽  
Author(s):  
V Valls-Bellés ◽  
MC Torres ◽  
P Muñiz ◽  
L Boix ◽  
ML González-Sanjose ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

scholarly journals Hesperetin protects SH-SY5Y cells against 6- hydroxydopamine-induced neurotoxicity via activation of NRF2/ARE signaling pathways

2020 ◽  
Vol 19 (6) ◽  
pp. 1197-1201 ◽  
Author(s):  
Jing Li ◽  
Yue Liu ◽  
Li Wang ◽  
Zhaowei Gu ◽  
Zhigang Huan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Viability ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Ldh Release ◽  
6 Hydroxydopamine

Purpose: To investigation the protective effects of hesperetin against 6-hydroxydopamine (6-OHDA)- induced neurotoxicity. Methods: SH-SY5Y cells were incubated with 6-OHDA to create an in vitro model of neurotoxicity. This model was used to test the neuroprotective effects of hesperetin. Cell viability was assessed by MTT and lactate dehydrogenase (LDH) release assays. Flow cytometry and western blot were used to quantify apoptosis. Oxidative stress was evaluated by determining intracellular glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS). Results: In SH-SY5Y cells, treatment with 6-OHDA decreased cell viability and promoted LDH release. However, exogenous hesperetin protected against 6-OHDA-mediated toxicity. Similarly, although incubation with 6-OHDA induced apoptosis and increased cleaved caspase-3 and -9 levels, treatment with hesperetin protected against these effects. Treatment with 6-OHDA also led to significant oxidative stress, as indicated by reduced GSH and SOD levels and increased MDA and ROS levels in SH-SY5Y cells. However, these changes were reversed by pre-treatment with hesperetin. Of interest, hesperetin led to changes in 6-OHDA-induced expression of NRF2, heme oxygenase-1 (HO-1), glutamate-cysteine ligase (GCL) catalytic subunit (GCLC), and GCL modulatory (GCLM). Conclusion: Hesperetin protects against cell toxicity, apoptosis, and oxidative stress via activation of NRF2 pathway in a 6-OHDA-induced model of neurotoxicity. Future studies should investigate the use of hesperetin as a potential therapeutic approach for prevention or management of Parkinson’s disease. Keywords: Hesperetin, 6-OHDA, Neurotoxicity, NRF2, Parkinson’s disease

Chinese Medicine PaBing-II Protects Human iPSC Derived Dopaminergic Neurons from Oxygen Stress

2021 ◽  
Author(s):  
Shouhai Wu ◽  
Tongxiang Lin ◽  
Yang Xu
Keyword(s):  
Oxidative Stress ◽  
Chinese Medicine ◽  
Pluripotent Stem Cells ◽  
Dopaminergic Neurons ◽  
Protective Effects ◽  
Midbrain Dopaminergic Neurons ◽  
Induced Pluripotent ◽  
6 Hydroxydopamine ◽  
Human Ipsc

Abstract BackgroundPaBing-II Formula (PB-II) is a traditional Chinese medicine developed to treat Parkinson's disease (PD). However, due to the complexity of PB-II and the difficulty of culturing human dopaminergic neurons (DAn) in vitro, the mechanism of PB-II to treat PD remains unclear. MethodsWe established the human induced pluripotent stem cells (iPSCs) and derived DAn from hiPSCs to study the protective effects of PB-II on DAn after oxidative stress, which plays an important role in PD pathogenesis. ResultsWe found that serum derived from rats that had ingested PB-II significantly protect hiPSC-derived DAn from reactive oxygen species (ROS). In addition, PB-II dependent serum can activate nuclear erythroid-derived factor 2 (Nrf2) responses, which are required for the neutralization of ROS. In addition, PB-II can activate the Nrf2/ARE signal pathway of midbrain dopaminergic neurons of PD rats induced with 6-hydroxydopamine (6-OHDA) injury, rescue DAn cells, and improve the symptoms of PD rats. ConclusionsPB-II significantly protects the DA neurons from oxidative stress by activating the Nrf2 pathway.

scholarly journals Neuroprotective and antioxidant activities of saponins’ mixture from Astragalus glycyphylloides in a model of 6-hydroxydopamine-induced oxidative stress on isolated rat brain synaptosomes

Pharmacia ◽  
2019 ◽  
Vol 66 (4) ◽  
pp. 233-236
Author(s):  
Magdalena Kondeva-Burdina ◽  
Ilina Krasteva ◽  
Georgi Popov ◽  
Vasil Manov
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Antioxidant Activities ◽  
Toxic Metabolite ◽  
Neuroprotective Effects ◽  
Rat Brain Synaptosomes ◽  
Brain Synaptosomes ◽  
6 Hydroxydopamine ◽  
Isolated Rat ◽  
Significant Concentration

The aim of the study was to investigate the possible neuroprotective and antioxidant activity of purified saponins’mixture (PSM), isolated from Astragalus glycyphylloides (Fabaceae), in a model of 6-hydroxydipamine (6-OHDA)-induced oxidative stress on isolated rat brain synaptosomes. Synaptosomes were incubated with 3 different concentrations of PSM: 60 µg/mL; 6 µg/mL; 0.6 µg/mL. The effects of PSM were compared to those of silymarin (S), at the same concentrations. The main parameters, characterized functional and metabolic status of synaptosomes, were investigated: viability (MTT-test) and level of reduced glutathione (GSH). At isolated rat brain synaptosomes, in conditions of 6-OHDA-induced oxidative stress (150 μМ), PSM revealed statistically significant, concentration-dependent, neuroprotective and antioxidant effects, compared to those of silymarin. Effects were most prominent at concentration 60 µg/mL. These neuroprotective effects of PSM might be due to the possible activity as scavenger of reactive oxygen species (ROS), produced by p-quinone (toxic metabolite of 6-OHDA).

scholarly journals Cytoprotective effects of silafibrate, a newly-synthesised siliconated derivative of clofibrate, against acetaminophen-induced toxicity in isolated rat hepatocytes

2014 ◽  
Vol 65 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Sara Nafisi ◽  
Reza Heidari ◽  
Mohammad Ghaffarzadeh ◽  
Mojtaba Ziaee ◽  
Hossein Hamzeiy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Inflammatory Responses ◽  
Liver Perfusion ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Cells ◽  
Isolated Rat Hepatocytes ◽  
Ros Formation ◽  
Isolated Rat

AbstractAcetaminophen (N-acetyl para amino phenol, APAP) is a widely used antipyretic and analgesic drug responsible for various drug-induced liver injuries. This study evaluated APAP-induced toxicity in isolated rat hepatocytes alongside the protective effects of silafibrate and N-acetyl cysteine (NAC). Hepatocytes were isolated from male Sprague-Dawley rats by collagenase enzyme perfusion via the portal vein. This technique is based on liver perfusion with collagenase after removing calcium ions (Ca2+) with a chelator. Cells were treated with different concentrations of APAP, silafibrate, and NAC. Cell death, reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial depolarisation were measured as toxicity markers. ROS formation and lipid peroxidation occurred after APAP administration to rat hepatocytes. APAP caused mitochondrial depolarisation in isolated cells. Administration of silafibrate (200 μmol L-1) and/or NAC (200 μmol L-1) reduced the ROS formation, lipid peroxidation, and mitochondrial depolarisation caused by APAP. Cytotoxicity induced by APAP in rat hepatocytes was mediated by oxidative stress. In addition, APAP seemed to target cellular mitochondria during hepatocyte damage. The protective properties of silafibrate and/or NAC against APAP‑induced hepatic injury may have involved the induction of antioxidant enzymes, protection against oxidative stress and inflammatory responses, and alteration in cellular glutathione content.

Sign in / Sign up

Export Citation Format

Share Document