Post treatment with Gastrodin suppresses oxidative stress and attenuates motor disorders following 6-OHDA induced Parkinson disease

Sadeghian, Zohre; Brooshghalan, Shahla Eyvari; Sabahi, Mohammadmahdi; Nourouzi, Nahal; Haddadi, Rasool

doi:10.1016/j.neulet.2022.136884

Cited by 13 publications

(3 citation statements)

References 57 publications

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“…Amount of LPO was determined by quantification of a thiobarbituric acid reagent. 36,37 LPO production react with thiobarbituric acid to produce a pink color with maximum absorption at 532 nm.…”

Section: Methodsmentioning

confidence: 99%

Anti-oxidative properties of nanocrocin in Zearalenone induced toxicity on Hek293 cell; The novel formulation and cellular assessment

et al. 2023

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Background Zearalenone (ZEA) is a mycotoxin produced by fungi and induces cytotoxicity by the generation of reactive oxygen species. The aim of this study was to evaluate and compare the nephroprotective effects of crocin and nano-crocin against ZEA-induced toxicity in HEK293 cell line via modulation of oxidative stress and special formulation to make nano-crocin. Method Nano-crocin physicochemical properties, such as size, load, appearance, and drug release profile were determined. Also, the viability of intoxicated HEK293 cells was evaluated by MTT assay. Furthermore, lactate dehydrogenase lipid Peroxidation (LPO), and oxidative stress biomarkers were measured. Result The best nano-crocin formulation with superior entrapment effectiveness (54.66 ± 6.02), more significant drug loading (1.89 ± 0.01), better zeta potential (−23.4 ± 2.844), and smaller particle size (140.3 ± 18.0 nm) was chosen. This study showed that treatment with crocin and nano-crocin in ZEA-induced cells, significantly decreased LDH and LPO levels and increased superoxide dismutase (SOD), catalase (CAT) activities, and total antioxidant capacity (TAC) levels compared to the control group. Moreover, nano-crocin had a more curative effect against oxidative stress than crocin. Conclusion Niosomal structure of crocin, when administered with the special formulation, may be more beneficial in reducing ZEA-induced in vitro toxicity than conventional crocin.

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Section: Methodsmentioning

confidence: 99%

Anti-oxidative properties of nanocrocin in Zearalenone induced toxicity on Hek293 cell; The novel formulation and cellular assessment

et al. 2023

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“…Rats were allowed to habituate to the experimental room for 60 min before both training and testing. Training and testing were performed between 10:00 AM and 1:00 PM [42].…”

Section: Rotarod Testmentioning

confidence: 99%

Restraint Stress Exacerbates Apoptosis in a 6-OHDA Animal Model of Parkinson Disease

et al. 2023

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Activation of the apoptotic pathway has been associated with promoting neuronal cell death in the pathophysiology of Parkinson disease (PD). Nonetheless, the mechanisms by which it may occurs remain unclear. It has been suggested that stress-induced oxidation and potentially apoptosis may play a major role in the progression of PD. Thus, in this study, we aimed to investigate the effect of subchronic restraint stress on striatal dopaminergic activity, iron, p53, caspase-3, and plasmatic acetylcholinesterase (AChE) levels in an animal model of PD induced by administration of 6-hydroxydopamine(6-OHDA) in the medial forebrain bundle (MFB). The obtained results showed that restraint stress exacerbates motor coordination de cits and anxiety in animals treated with 6-OHDA in comparison to animals receiving saline, and it had no effect on object recognition memory.On another hand, 6-OHDA decreased dopamine(DA) levels, increased iron accumulation, and induced overexpression of the pro-apoptotic factors caspase-3, p53, and AChE. More interestingly, post-lesion restraint stress exacerbated the expression of caspase-3 and AChE without affecting p53 expression.These ndings suggest that subchronic stress may accentuate apoptosis and may contribute to DA neuronal loss in the striatal regions and possibly exacerbate the progression of PD.

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“…Gastrodin treatment has been shown to decrease Aβ-induced cell death and decrease lactic dehydrogenase release in primary cultured neuronal cells [40]. In addition, gastrodin exerts antioxidant, mitochondrial protection [41,42] and anti-inflammatory activities [32,34,[41][42][43][44][45]. Several signaling pathways have been found mediating the effect of gastrodin in these studies, including nuclear factor-E2-related factor 2 (Nrf2), extracellular regulated kinase (ERK) 1/2, mitogen activated protein kinase (MAPK) and glycogen synthase kinase-3β (GSK-3β) [26,28,34,37,43,[46][47][48][49][50].…”

Section: Introductionmentioning

confidence: 99%

Gastrodin ameliorates synaptic impairment, reestablishes mitochondrial membrane potential and reduces oxidative stress in N2a/APP cells through ERK1/2 and GSK-3β pathways

Tang

Peng

Wang

et al. 2023

Preprint

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Alzheimer's disease (AD) is featured by abnormal &beta-amyloid (Abeta) deposition, neurofibrillary tangle formation, downstream mitochondrial dysfunction, oxidative stress, and synaptic loss. Gastrodin, a phenolic glycoside, has shown neuroprotective effect and used in the treatment of a range of brain diseases. Here we aim to assess the mechanisms and signaling pathways involved in the neuroprotective effect of gastrodin in murine neuroblastoma N2a cells expressing human Swedish mutant amyloid precursor protein (N2a/APP). The levels of pre- and postsynaptic proteins, amyloid precursor protein C-terminal fragments (APP-CTFs), levels of tau, glycogen synthase kinase-3beta (GSK-3beta), extracellular regulated kinase (ERK), and c-Jun N-terminal Kinase (JNK) were assessed by Western blotting. Flow cytometry assays for mitochondrial membrane potential (JC1) and reactive oxidative stress, as well as immunofluorescence staining for lipid peroxidation (4-hydroxynonenal) and DNA oxidation (8-hydroxy-2'-deoxyguanosine), were performed. We found that gastrodin treatment increased the levels of presynaptic SNAP25, synaptophysin, and postsynaptic PSD95, reduced phosphorylated tau protein Ser396, and APP-CTFs in N2a/APP cells. In addition, gastrodin reduced the levels of reactive oxygen species generation, lipid peroxidation, and DNA oxidation, reestablished mitochondrial membrane potential. Upregulated levels of phosphorylated-GSK-3beta, reduced levels of phosphorylated-ERK, and phosphorylated-JNK were involved the protective effect of gastrodin. In conclusion, we demonstrated a neuroprotective effect of gastrodin in N2a/APP cell line.

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Post treatment with Gastrodin suppresses oxidative stress and attenuates motor disorders following 6-OHDA induced Parkinson disease

Cited by 13 publications

References 57 publications

Anti-oxidative properties of nanocrocin in Zearalenone induced toxicity on Hek293 cell; The novel formulation and cellular assessment

Anti-oxidative properties of nanocrocin in Zearalenone induced toxicity on Hek293 cell; The novel formulation and cellular assessment

Restraint Stress Exacerbates Apoptosis in a 6-OHDA Animal Model of Parkinson Disease

Gastrodin ameliorates synaptic impairment, reestablishes mitochondrial membrane potential and reduces oxidative stress in N2a/APP cells through ERK1/2 and GSK-3β pathways

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