scholarly journals Resveratrol in Rodent Models of Parkinson’s Disease: A Systematic Review of Experimental Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Cheng-Fu Su ◽  
Li Jiang ◽  
Xiao-Wen Zhang ◽  
Ashok Iyaswamy ◽  
Min Li

Parkinson’s disease (PD) is a common neurodegenerative disease featured by progressive degeneration of nigrostriatal dopaminergic neurons (DA) accompanied with motor function impairment. Accumulating evidence has demonstrated that natural compounds from herbs have potent anti-PD efficacy in PD models. Among those compounds, resveratrol, a polyphenol found in many common plants and fruits, is more effective against PD. Resveratrol has displayed a potent neuroprotective efficacy in several PD animal models. However, there is still no systematic analysis of the quality of methodological design of these studies, nor of their results. In this review, we retrieved and analyzed 18 studies describing the therapeutic effect of resveratrol on PD animal models. There are 5 main kinds of PD rodent models involved in the 18 articles, including chemical-induced (MPTP, rotenone, 6-OHDA, paraquat, and maneb) and transgenic PD models. The neuroprotective mechanisms of resveratrol were mainly concentrated on the antioxidation, anti-inflammation, ameliorating mitochondrial dysfunction, and motor function. We discussed the disadvantages of different PD animal models, and we used meta-analysis approach to evaluate the results of the selected studies and used SYRCLE’s risk of bias tool to evaluate the methodological quality. Our analytical approach minimized the bias of different studies. We have also summarized the pharmacological mechanisms of resveratrol on PD models as reported by the researchers. The results of this study support the notion that resveratrol has significant neuroprotective effects on different PD models quantified using qualitative and quantitative methods. The collective information in our review can guide researchers to further plan their future experiments without any hassle regarding preclinical and clinical studies. In addition, this collective assessment of animal studies can provide a qualitative analysis of different PD animal models, either to guide further testing of these models or to avoid unnecessary duplication in their future research.

2018 ◽  
Vol 17 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Abdelrahman Ibrahim Abushouk ◽  
Ahmed Negida ◽  
Rasha Abdelsalam Elshenawy ◽  
Hossam Zein ◽  
Ali M. Hammad ◽  
...  

Parkinson's disease (PD) is the most prevalent movement disorder in the world. The major pathological hallmarks of PD are death of dopaminergic neurons and the formation of Lewy bodies. At the moment, there is no cure for PD; current treatments are symptomatic. Investigators are searching for neuroprotective agents and disease modifying strategies to slow the progress of neurodegeneration. However, due to lack of data about the main pathological sequence of PD, many drug targets failed to provide neuroprotective effects in human trials. Recent evidence suggests the involvement of C-Abelson (c-Abl) tyrosine kinase enzyme in the pathogenesis of PD. Through parkin inactivation, alpha synuclein aggregation, and impaired autophagy of toxic elements. Experimental studies showed that (1) c-Abl activation is involved in neurodegeneration and (2) c-Abl inhibition shows neuroprotective effects and prevents dopaminergic neuronal' death. Current evidence from experimental studies and the first in-human trial shows that c-Abl inhibition holds the promise for neuroprotection against PD and therefore, justifies the movement towards larger clinical trials. In this review article, we discussed the role of c-Abl in PD pathogenesis and the findings of preclinical experiments and the first in-human trial. In addition, based on lessons from the last decade and current preclinical evidence, we provide recommendations for future research in this area.


2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Keya Li ◽  
Xinyue Li ◽  
Guiying Shi ◽  
Xuepei Lei ◽  
Yiying Huang ◽  
...  

AbstractAnimal models provide an opportunity to assess the optimal treatment way and the underlying mechanisms of direct clinical application of adipose-derived stem cells (ADSCs). Previous studies have evaluated the effects of primitive and induced ADSCs in animal models of Parkinson’s disease (PD). Here, eight databases were systematically searched for studies on the effects and in vivo changes caused by ADSC intervention. Quality assessment was conducted using a 10-item risk of bias tool. For the subsequent meta-analysis, study characteristics were extracted and effect sizes were computed. Ten out of 2324 published articles (n = 169 animals) were selected for further meta-analysis. After ADSC therapy, the rotation behavior (10 experiments, n = 156 animals) and rotarod performance (3 experiments, n = 54 animals) were improved (P < 0.000 01 and P = 0.000 3, respectively). The rotation behavior test reflected functional recovery, which may be due to the neurogenesis from neuronally differentiated ADSCs, resulting in a higher pooled effect size of standard mean difference (SMD) (− 2.59; 95% CI, − 3.57 to − 1.61) when compared to that of primitive cells (− 2.18; 95% CI, − 3.29 to − 1.07). Stratified analyses by different time intervals indicated that ADSC intervention exhibited a long-term effect. Following the transplantation of ADSCs, tyrosine hydroxylase-positive neurons recovered in the lesion area with pooled SMD of 13.36 [6.85, 19.86]. Transplantation of ADSCs is a therapeutic option that shows long-lasting effects in animal models of PD. The potential mechanisms of ADSCs involve neurogenesis and neuroprotective effects. The standardized induction of neural form of transplanted ADSCs can lead to a future application in clinical practice.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Raymond Li ◽  
Ann Jose ◽  
Jessica Poon ◽  
Cindy Zou ◽  
Maria Istafanos ◽  
...  

Abstract Context Parkinson’s disease (PD) is a neurodegenerative disease that leads to impaired motor and non-motor function in patients. PD is non-curative and gradually reduces quality of life, leading patients to seek treatment for symptom management. Osteopathic manipulative treatment (OMT) applies the biomechanical, neurologic, circulatory, metabolic, and psychosocial models in approaching and treating the major symptomatology of PD patients. Objectives This article evaluates the literature published in the past 10 years analyzing evidence on OMT and its functional application on gait, balance, motor function, bradykinesia, and autonomic dysfunctions, and to identify promising avenues for further investigation. Methods The authors obtained studies from the research databases MEDLINE/PubMed, ScienceDaily, and EBSCO, as well as the Journal of American Osteopathic Association’s published archives. Searches were conducted in December 2020 utilizing the search phrases “OMM” (osteopathic manipulative medicine), “OMT,” “osteopathic,” “Parkinson Disease,” “manual therapy,” “physical therapy,” “training,” “autonomics,” “gait,” and “balance.” Articles published between 2010 and 2021 including subjects with Parkinson’s disease and the use of OMT or any other form of manual therapy were included. Five authors independently performed literature searches and methodically resolved any disagreements over article selection together. Results There were a total of 10,064 hits, from which 53 articles were considered, and five articles were selected based on the criteria. Conclusions The progressive nature of PD places symptom management on the forefront of maintaining patients’ quality of life. OMT has demonstrated the greatest efficacy on managing motor-related and neurologic symptoms and assists in treating the greater prevalence of somatic dysfunctions that arise from the disease. Research in this field remains limited and should be the target of future research.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Michel Rijntjes

This review contains a critical appraisal of current knowledge about the use of beans in both animal models and patients with Parkinson’s disease (PD). The potential beneficial effects of beans in PD are increasingly being touted, not only in scientific journals but also by the lay media. While there is a long tradition in Ayurvedic medicine of prescribing extracts from Mucuna pruriens (MP), whose seeds contain 5% L-3,4-dihydroxyphenylalanin (L-DOPA), many other beans also contain L-DOPA (broad beans, common beans, and soybeans) or have other ingredients (coffee and cocoa) that may benefit PD patients. Indeed, bean-derived compounds can elicit neuroprotective effects in animal models of PD, while several studies in human PD patients have shown that motor performance can improve after ingestion of bean extracts. However, there are several arguments countering the view that beans serve as a natural therapy for PD: (i) the results from animal PD models are not necessarily directly applicable to humans; (ii) beans have many bioactive ingredients, some of which can be harmful in large doses; (iii) studies in human PD patients are scarce and only report on the effects of single doses or the administration of bean extract over short periods of time; and (iv) no data on long-term efficacy or side effects of bean therapy are available. Therefore, reservations about the use of beans as a “natural” therapy for PD seem to be justified.


PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3933 ◽  
Author(s):  
Justin Y.D. Lu ◽  
Ping Su ◽  
James E.M. Barber ◽  
Joanne E. Nash ◽  
Anh D. Le ◽  
...  

Clinical evidence points to neuroprotective effects of smoking in Parkinson’s disease (PD), but the molecular mechanisms remain unclear. We investigated the pharmacological pathways involved in these neuroprotective effects, which could provide novel ideas for developing targeted neuroprotective treatments for PD. We used the ETC complex I inhibitor methylpyridinium ion (MPP+) to induce cell death in SH-SY5Y cells as a cellular model for PD and found that nicotine inhibits cell death. Using choline as a nicotinic acetylcholine receptor (nAChR) agonist, we found that nAChR stimulation was sufficient to protect SH-SY5Y cells against cell death from MPP+. Blocking α7 nAChR with methyllycaconitine (MLA) prevented the protective effects of nicotine, demonstrating that these receptors are necessary for the neuroprotective effects of nicotine. The neuroprotective effect of nicotine involves other pathways relevant to PD. Cleaved Poly (ADP-ribose) polymerase-1 (PARP-1) and cleaved caspase-3 were decreased by nicotine in 6-hydroxydopamine (6-OHDA) lesioned mice and in MPP+-treated SH-SY5Y cells. In conclusion, our data indicate that nicotine likely exerts neuroprotective effects in PD through the α7 nAChR and downstream pathways including PARP-1 and caspase-3. This knowledge could be pursued in future research to develop neuroprotective treatments for PD.


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