Bibliometrics and Visualization of the Mechanisms of Parkinson's Diseases Based on Animal Models

Objective: Energy metabolism disorder is one of the causes of Parkinson's disease (PD). Rodents, such as rats and mice are often used to establish animal models of PD. This paper used a bibliometric method to analyze the studies of rat and mouse PD models published between 2009 and 2018 in the Web of Science (WOS) database using CiteSpace V software. In addition, we conducted a literature review on the development status and research hotspots in this field in the past ten years. Methods: The related articles on rat and mouse PD models were retrieved from the WOS database, and an analysis of the keywords in these articles was conducted using CiteSpace V. A timeline graph was developed by the software in order to show the focus of researchers in the PD field. Results : A total of 8,636 articles were obtained. Results of the cluster analysis in the PD field such as neuroinflammation, oxidative stress, and autophagy, contributed to the systematic review about the pathogenesis of PD. At the same time, based on the property of the model drug, this review has summarized and compared different administration techniques and mechanisms of 6-hydroxydopamine (6- OHDA), 1-methyl-4-phenyl-1, 2, 4, 5-tetrahydropyridine (MPTP), paraquat and rotenone. Conclusion: According to the bibliometric analysis, studies on PD were focused on the mechanisms of oxidative stress, neuroinflammation, and autophagy. Activated microglia releases inflammatory cytokines; mitochondrial dysfunction is caused by oxidative damage of mitochondrial protein; abnormal autophagy-lysosome pathway can lead to abnormal protein deposition in dopaminergic neurons. In addition, although many animal models of PD have been established, there are some limitations of such models. Therefore, it is necessary to develop models that accurately mimic human PD.

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Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

Parkinson s Disease ◽

10.4061/2011/307875 ◽

2011 ◽

Vol 2011 ◽

pp. 1-9 ◽

Cited By ~ 6

Author(s):

Kyota Fujita ◽

Yusaku Nakabeppu ◽

Mami Noda

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Animal Models ◽

Animal Studies ◽

Clinical Symptoms ◽

Therapeutic Effects ◽

Therapeutic Approaches ◽

Cellular Apoptosis ◽

6 Hydroxydopamine

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

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Prevention or Amelioration of Autism-Like Symptoms in Animal Models: Will it Bring Us Closer to Treating Human ASD?

International Journal of Molecular Sciences ◽

10.3390/ijms20051074 ◽

2019 ◽

Vol 20 (5) ◽

pp. 1074 ◽

Cited By ~ 12

Author(s):

Asher Ornoy ◽

Liza Weinstein-Fudim ◽

Zivanit Ergaz

Keyword(s):

Oxidative Stress ◽

Animal Models ◽

Animal Studies ◽

Autism Spectrum ◽

Experimental Animal Models ◽

Genetic Manipulations ◽

Children With Asd ◽

Brain Neurotransmitters ◽

Brain Oxidative Stress ◽

Rats And Mice

Since the first animal model of valproic acid (VPA) induced autistic-like behavior, many genetic and non-genetic experimental animal models for Autism Spectrum Disorder (ASD) have been described. The more common non-genetic animal models induce ASD in rats and mice by infection/inflammation or the prenatal or early postnatal administration of VPA. Through the establishment of these models, attempts have been made to ameliorate or even prevent ASD-like symptoms. Some of the genetic models have been successfully treated by genetic manipulations or the manipulation of neurotransmission. Different antioxidants have been used (i.e., astaxanthin, green tea, piperine) to reduce brain oxidative stress in VPA-induced ASD models. Agents affecting brain neurotransmitters (donepezil, agmatine, agomelatine, memantine, oxytocin) also successfully reduced ASD-like symptoms. However, complete prevention of the development of symptoms was achieved only rarely. In our recent study, we treated mouse offspring exposed on postnatal day four to VPA with S-adenosine methionine (SAM) for three days, and prevented ASD-like behavior, brain oxidative stress, and the changes in gene expression induced by VPA. In this review, we describe, in addition to our data, the existing literature on the prevention/amelioration of ASD-like symptoms. We also discuss the possible mechanisms underlying some of these phenomena. Finally, we describe some of the clinical trials in children with ASD that were carried out as a result of data from animal studies, especially those with polyunsaturated fatty acids (PUFAs).

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Extraction of breviscapine from Erigeron breviscapus and its effect on oxidative stress, inflammation, energy metabolism disorder and apoptosis in rats with uterine ischemia-reperfusion injury

Food Science and Technology ◽

10.1590/fst.31421 ◽

2021 ◽

Author(s):

Yunxiu ZHAO ◽

Yongzhen ZHANG ◽

Yanyan ZHANG ◽

Bing HAN ◽

Huan CHANG ◽

...

Keyword(s):

Oxidative Stress ◽

Energy Metabolism ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Metabolism Disorder ◽

Erigeron Breviscapus ◽

Energy Metabolism Disorder

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Psoralen Induces Developmental Toxicity in Zebrafish Embryos/Larvae Through Oxidative Stress, Apoptosis, and Energy Metabolism Disorder

Frontiers in Pharmacology ◽

10.3389/fphar.2018.01457 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 12

Author(s):

Qing Xia ◽

Lingying Wei ◽

Yun Zhang ◽

Haotian Kong ◽

Yongping Shi ◽

...

Keyword(s):

Oxidative Stress ◽

Energy Metabolism ◽

Developmental Toxicity ◽

Zebrafish Embryos ◽

Metabolism Disorder ◽

Energy Metabolism Disorder

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Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

Biomolecules ◽

10.3390/biom10010146 ◽

2020 ◽

Vol 10 (1) ◽

pp. 146 ◽

Cited By ~ 2

Author(s):

Fei-Xuan Wang ◽

Hong-Yan Li ◽

Yun-Qian Li ◽

Ling-Dong Kong

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Medicinal Plants ◽

Bioactive Compounds ◽

Lipid Peroxidation Product ◽

Metabolism Disorder ◽

Human Disorders ◽

Eye Damage ◽

Peroxidation Product ◽

Energy Metabolism Disorder

The toxic reactive aldehyde 4-hydroxynonenal (4-HNE) belongs to the advanced lipid peroxidation end products. Accumulation of 4-HNE and formation of 4-HNE adducts induced by redox imbalance participate in several cytotoxic processes, which contribute to the pathogenesis and progression of oxidative stress-related human disorders. Medicinal plants and bioactive natural compounds are suggested to be attractive sources of potential agents to mitigate oxidative stress, but little is known about the therapeutic potentials especially on combating 4-HNE-induced deleterious effects. Of note, some investigations clarify the attenuation of medicinal plants and bioactive compounds on 4-HNE-induced disturbances, but strong evidence is needed that these plants and compounds serve as potent agents in the prevention and treatment of disorders driven by 4-HNE. Therefore, this review highlights the pharmacological basis of these medicinal plants and bioactive compounds to combat 4-HNE-induced deleterious effects in oxidative stress-related disorders, such as neurotoxicity and neurological disorder, eye damage, cardiovascular injury, liver injury, and energy metabolism disorder. In addition, this review briefly discusses with special attention to the strategies for developing potential therapies by future applications of these medicinal plants and bioactive compounds, which will help biological and pharmacological scientists to explore the new vistas of medicinal plants in combating 4-HNE-induced deleterious effects.

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Research on the Species Difference of the Hepatotoxicity of Medicine Based on Transcriptome

Frontiers in Pharmacology ◽

10.3389/fphar.2021.647084 ◽

2021 ◽

Vol 12 ◽

Author(s):

Ziying Xu ◽

Qianjun Kang ◽

Zihui Yu ◽

Lichun Tian ◽

Jingxuan Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Animal Models ◽

Liver Injury ◽

Drug Toxicity ◽

Species Difference ◽

Sprague Dawley ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Rats And Mice

In recent years, several drugs have been withdrawn from use by regulatory bodies owing to hepatotoxicity; therefore, studies on drug-induced liver injury (DILI) are being actively pursued. Most studies evaluating DILI use rats or mice as animal models to determine drug toxicity; however, the toxicity of a drug can vary between rats or mice. These inconsistencies in in vivo studies among different animal models affect the extrapolation of experimental results to humans. Thus, it is particularly important to choose the most suitable animal model to determine drug hepatotoxicity owing to the genomic differences between rats and mice resulting from evolution. In this study, genome-wide transcriptome analysis was used to explore hepatotoxicity caused by differences in species. Our findings provide the preclinical basis to further study the mechanisms of drug hepatotoxicity and aid in the selection of animal models to determine drug safety. We used murine models (Sprague-Dawley and Wistar rats, ICR and Kunming mice) in this study and by using transcriptome sequencing with the differentially expressed genes in rat and mouse livers as the entry point, we explored the mechanism of oxidative stress and the difference in gene expression in the lipid-metabolism pathway between rats and mice. The clinically established hepatotoxic drugs, fructus psoraleae and acetaminophen were used to validate our study. Using pathological studies, we confirmed that oxidative stress in mice was more serious than that in rats, and that Kunming mice were more suited for the study of oxidative stress-related DILI. The validity of our findings was further verified based on gene expression. Thus, our study could serve as a valuable reference for the evaluation of potential preclinical hepatotoxicity. Moreover, it could be used in the prediction and early diagnosis of drug-induced liver injury caused by traditional Chinese medicine or synthetic drugs, thereby providing a new avenue for drug-toxicity studies.

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Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models

International Journal of Molecular Sciences ◽

10.3390/ijms22041514 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1514 ◽

Cited By ~ 1

Author(s):

Akihiro Yachie

Keyword(s):

Oxidative Stress ◽

Animal Models ◽

Heme Oxygenase ◽

Inflammatory Diseases ◽

Cell Types ◽

Pharmacological Intervention ◽

Heme Oxygenase 1 ◽

Inflammatory Reactions

Since Yachie et al. reported the first description of human heme oxygenase (HO)-1 deficiency more than 20 years ago, few additional human cases have been reported in the literature. A detailed analysis of the first human case of HO-1 deficiency revealed that HO-1 is involved in the protection of multiple tissues and organs from oxidative stress and excessive inflammatory reactions, through the release of multiple molecules with anti-oxidative stress and anti-inflammatory functions. HO-1 production is induced in vivo within selected cell types, including renal tubular epithelium, hepatic Kupffer cells, vascular endothelium, and monocytes/macrophages, suggesting that HO-1 plays critical roles in these cells. In vivo and in vitro studies have indicated that impaired HO-1 production results in progressive monocyte dysfunction, unregulated macrophage activation and endothelial cell dysfunction, leading to catastrophic systemic inflammatory response syndrome. Data from reported human cases of HO-1 deficiency and numerous studies using animal models suggest that HO-1 plays critical roles in various clinical settings involving excessive oxidative stress and inflammation. In this regard, therapy to induce HO-1 production by pharmacological intervention represents a promising novel strategy to control inflammatory diseases.

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