scholarly journals Anti-inflammatory and Anti-oxidant Activity of Hidrox® in Rotenone-Induced Parkinson’s Disease in Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 824 ◽  
Author(s):  
Rosalba Siracusa ◽  
Maria Scuto ◽  
Roberta Fusco ◽  
Angela Trovato ◽  
Maria Laura Ontario ◽  
...  

Background: In developed countries, the extension of human life is increasingly accompanied by a progressive increase in neurodegenerative diseases, most of which do not yet have effective therapy but only symptomatic treatments. In recent years, plant polyphenols have aroused considerable interest in the scientific community. The mechanisms currently hypothesized for the pathogenesis of Parkinson’s disease (PD) are neuroinflammation, oxidative stress and apoptosis. Hydroxytyrosol (HT), the main component of Hidrox® (HD), has been shown to have some of the highest free radical evacuation and anti-inflammatory activities. Here we wanted to study the role of HD on the neurobiological and behavioral alterations induced by rotenone. Methods: A study was conducted in which mice received HD (10 mg/kg, i.p.) concomitantly with rotenone (5 mg/kg, o.s.) for 28 days. Results: Locomotor activity, catalepsy, histological damage and several characteristic markers of the PD, such as the dopamine transporter (DAT) content, tyrosine hydroxylase (TH) and accumulation of α-synuclein, have been evaluated. Moreover, we observed the effects of HD on oxidative stress, neuroinflammation, apoptosis and inflammasomes. Taken together, the results obtained highlight HD’s ability to reduce the loss of dopaminergic neurons and the damage associated with it by counteracting the three main mechanisms of PD pathogenesis. Conclusion: HD is subject to fewer regulations than traditional drugs to improve patients’ brain health and could represent a promising nutraceutical choice to prevent PD.

2020 ◽  
Author(s):  
Lingling Jiao ◽  
Fengju Jia ◽  
Xixun Du ◽  
Pei Zhang ◽  
Yong Li ◽  
...  

Abstract BackgroundGhrelin has been identified as a multifunctional peptide that has many potential applications for the treatment of various diseases, including Parkinson’s disease (PD). However, little is known about the pathophysiological function and mechanism of ghrelin in PD. MethodELISA was used for detecting plasma total and active ghrelin levels, dopamine (DA) content was measured by HPLC-ECD, immunofluorescence staining and Western blot were used to detect protein expressions, and cytokine was tested by Bio-PlexPro™ assay.ResultsHere, we reported a PD model that overexpressing mutant human A53T α-syn mice exhibited a decreased levels of total and active ghrelin in plasma, fewer tyrosine hydroxylase (TH)-positive neurons in the substantia nigra (SN), lower DA content in the striatum (Str), and less weight. These changes were rescued by the subcutaneous administration of low-dose ghrelin. Interestingly, ghrelin had no effect on weight gain in wild-type mice but improved weight loss in A53T mice. In addition, ghrelin administration also attenuated the decreased Bcl-2/Bax ratio and superoxide dismutase1 (SOD1) protein levels and inhibited the upregulation pro-inflammatory cytokine interleukin-6 (IL-6) and tumour necrosis factor a (TNFa) and the downregulation of anti-inflammatory cytokine IL-10. In addition, ghrelin inhibited the increase in Iba1-positive cells in mice with PD.ConclusionsHere we reported that ghrelin had a protective effect on dopaminergic neurons and against weight loss from PD via anti-oxidant, anti-inflammatory and anti-apoptotic mechanisms, which suggested that ghrelin could be an endogenous protective factor that prevents the onset or the progression of PD.


2021 ◽  
Vol 22 (4) ◽  
pp. 2098
Author(s):  
Seulah Lee ◽  
Yeon Ji Suh ◽  
Seonguk Yang ◽  
Dong Geun Hong ◽  
Akihito Ishigami ◽  
...  

Oxidative stress, mitochondrial dysfunction, and neuroinflammation are strongly associated with the pathogenesis of Parkinson’s disease (PD), which suggests that anti-oxidative and anti-inflammatory compounds might provide an alternative treatment for PD. Here, we evaluated the neuroprotective effects of evernic aid (EA), which was screened from a lichen library provided by the Korean Lichen Research Institute at Sunchon National University. EA is a secondary metabolite generated by lichens, including Ramalina, Evernia, and Hypogymnia, and several studies have described its anticancer, antifungal, and antimicrobial effects. However, the neuroprotective effects of EA have not been studied. We found that EA protected primary cultured neurons against 1-methyl-4-phenylpyridium (MPP+)-induced cell death, mitochondrial dysfunction, and oxidative stress, and effectively reduced MPP+-induced astroglial activation by inhibiting the NF-κB pathway. In vivo, EA ameliorated MPTP-induced motor dysfunction, dopaminergic neuronal loss, and neuroinflammation in the nigrostriatal pathway in C57BL/6 mice. Taken together, our findings demonstrate that EA has neuroprotective and anti-inflammatory effects in PD models and suggest that EA is a potential therapeutic candidate for PD.


2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Ovidiu-Dumitru Ilie ◽  
Alin Ciobica ◽  
Jack McKenna ◽  
Bogdan Doroftei ◽  
Ioannis Mavroudis

The aetiology of Parkinson’s disease (PD) is a highly debated topic. Despite the progressive increase in the number of patients diagnosed with PD over the last couple of decades, the causes remain largely unknown. This report is aimed at highlighting the main features of the microbial communities which have been termed “the second brain” that may be a major participant in the etiopathophysiology of PD. It is possible that dysbiosis could be caused by an overactivity of proinflammatory cytokines which act on the gastrointestinal tract as well as infections. The majority of patients who are diagnosed with PD display gastrointestinal symptoms as one of the earliest features. In addition, an unbalanced cycle of oxidative stress caused by dysbacteriosis may have the effect of gradually promoting PD’s specific phenotype. Thus, it seems that bacteria possess the ability to manipulate the brain by initiating specific responses, defining their capability to configure the human body, with oxidative stress playing a pivotal role in preventing infections but also in activating related signalling pathways.


2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Kecheng Lei ◽  
Yijue Shen ◽  
Yijing He ◽  
Liwen Zhang ◽  
Jingxing Zhang ◽  
...  

Parkinson’s disease (PD) is a neurodegenerative disease characterized by the gradual loss of dopaminergic (DA) neurons in the substantia nigra (SN) and the formation of intracellular Lewy bodies (LB) in the brain, which aggregates α-synuclein (α-Syn) as the main component. The interest of flavonoids as potential neuroprotective agents is increasing due to its high efficiency and low side effects. Baicalin is one of the flavonoid compounds, which is a predominant flavonoid isolated from Scutellaria baicalensis Georgi. However, the key molecular mechanism by which Baicalin can prevent the PD pathogenesis remains unclear. In this study, we used bioinformatic assessment including Gene Ontology (GO) to elucidate the correlation between oxidative stress and PD pathogenesis. RNA-Seq methods were used to examine the global expression profiles of noncoding RNAs and found that C/EBPβ expression was upregulated in PD patients compared with healthy controls. Interestingly, Baicalin could protect DA neurons against reactive oxygen species (ROS) and decreased C/EBPβ and α-synuclein expression in pLVX-Tet3G-α-synuclein SH-SY5Y cells. In a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD mouse model, the results revealed that treatment with Baicalin improved the PD model’s behavioral performance and reduced dopaminergic neuron loss in the substantia nigra, associated with the inactivation of proinflammatory cytokines and oxidative stress. Hence, our study supported that Baicalin repressed C/EBPβ via redox homeostasis, which may be an effective potential treatment for PD.


2012 ◽  
Vol 11 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Marcella Reale ◽  
Mirko Pesce ◽  
Medha Priyadarshini ◽  
Mohammad A Kamal ◽  
Antonia Patruno

2021 ◽  
Vol 22 (9) ◽  
pp. 4676
Author(s):  
Katja Badanjak ◽  
Sonja Fixemer ◽  
Semra Smajić ◽  
Alexander Skupin ◽  
Anne Grünewald

With the world’s population ageing, the incidence of Parkinson’s disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.


2015 ◽  
Vol 9 ◽  
Author(s):  
Javier Blesa ◽  
Ines Trigo-Damas ◽  
Anna Quiroga-Varela ◽  
Vernice R. Jackson-Lewis

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