scholarly journals Down-regulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Qing Shi ◽  
Yuanjiao Zhang ◽  
Junting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
The Central Nervous System ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In C. elegans worms, down-regulated RPS-30 plays a defensive role against damage due to oxidative stress for worm survival by regulating ced-3 down-regulated. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-RPS-30 down-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

scholarly journals Down-regulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Author(s):  
Wei-Wei Sun ◽  
Xiu-Mei Yan ◽  
Qing Shi ◽  
Yuan-Jiao Zhang ◽  
Jun-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
The Central Nervous System ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30–/– mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30–/– mutant worms.Conclusion: In C. elegans worms, down-regulated RPS-30 plays a defensive role against damage due to oxidative stress for worm survival by regulating ced-3 down-regulated. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-RPS-30 down-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

scholarly journals Down-regulated RPS-30 in Angiostrongylus Cantonensis L5 Plays a Defensive Role Against Damage Due to Oxidative Stress

2020 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Qing Shi ◽  
Yuanjiao Zhang ◽  
Junting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Structural Characterisation ◽  
C Elegans ◽  
Homologous Protein ◽  
Defensive Role ◽  
Helminthic Infections ◽  
High Level

Abstract Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; oxidative stress assay was used to determine the functions of Acan-RPS-30.Results: Our results showed that Acan-RPS-30 consisted of 130 amino acids, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In A. cantonensis L5 worms, down-regulated Acan-RPS-30 plays a defensive role against damage due to oxidative stress for worm survival through inhibiting apoptosis by regulating ced-3 down-regulated.

scholarly journals Downregulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Wei-Wei Sun ◽  
Xiu-Mei Yan ◽  
Qing Shi ◽  
Yuan-Jiao Zhang ◽  
Jun-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
C Elegans ◽  
Defensive Role ◽  
The Central Nervous System ◽  
Rapid Amplification ◽  
Apoptosis Gene ◽  
High Level

Abstract Background Eosinophilic meningitis, caused by fifth-stage larvae of the nematode (roundworm) Angiostrongylus cantonensis, is mainly attributed to the contribution of eosinophils to tissue inflammatory responses in helminthic infections. Eosinophils are associated with the killing of helminths via peroxidative oxidation and hydrogen peroxide generated by the dismutation of superoxide produced during respiratory bursts. In contrast, when residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in the hosts. In a previous study we demonstrated that the expression of the A. cantonensis RPS 30 gene (Acan-rps-30) was significantly downregulated in A. cantonensis L5 roundworms residing in cerebrospinal fluid with a high level of eosinophils. Acan-RPS-30 is a protein homologous to the human Fau protein that plays a pro-apoptotic regulatory role and may function in protecting worms from oxidative stress. Methods The isolation and structural characterization of Acan-RPS-30 were performed using rapid amplification of cDNA ends (RACE), genome walking and bioinformatics. Quantitative real-time-PCR and microinjection were used to detect the expression patterns of Acan-rps-30. Feeding RNA interference (RNAi) was used to knockdown the apoptosis gene ced-3. Microinjection was performed to construct transgenic worms. An oxidative stress assay was used to determine the functions of Acan-RPS-30. Results Our results showed that Acan-RPS-30 consisted of 130 amino acids. It was grouped into clade V with C. elegans in the phylogenetic analysis. It was expressed ubiquitously in worms and was downregulated in both L5 larvae and adult A. cantonensis. Worms expressing pCe-rps30::Acan-rps-30::rfp, with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes ced-3 and ced-4 were both upregulated in the transgenic worms. The phenotype susceptible to oxidative stress could be converted with a ced-3 defective mutation and RNAi. rps-30−/− mutant worms were resistant to oxidative stress, with ced-3 and ced-4 both downregulated. The oxidative stress-resistant phenotype could be rescued and inhibited by through the expression of pCe-rps30::Acan-rps-30::rfp in rps-3−/− mutant worms. Conclusion In C. elegans worms, downregulated RPS-30 plays a defensive role against damage due to oxidative stress, facilitating worm survival by regulating downregulated ced-3. This observation may indicate the mechanism by which A. cantonensis L5 worms, with downregulated Acan-RPS-30, survive in the central nervous system of humans from the immune response of eosinophils. Graphic abstract

scholarly journals Up-Regulated Galectin-1 in Angiostrongylus Cantonensis L5 Reduces Body Fat and Increases Oxidative Stress Tolerance

2021 ◽  
Author(s):  
Weiwei Sun ◽  
Xiumei Yan ◽  
Aijun Qiao ◽  
Yuanjiao Zhang ◽  
Ling Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Stress Tolerance ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Angiostrongylus Cantonensis ◽  
Lipid Deposition ◽  
Oxidative Stress Tolerance ◽  
The Central Nervous System

Abstract Background: Angiostrongylus cantonensis L5, parasitizing in human cerebrospinal fluid, leads to eosinophilic meningitis, which is attributed to tissue inflammatory responses caused primarily by high percentage of eosinophils. Eosinophils are also involved in helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival. In previous study, we have demonstrated the extracellular function of Acan-Gal-1 in inducing the apoptosis of macrophages. And here, the intracellular functions of Acan-Gal-1 were investigated with the aim to further reveal the mechanism of A. cantonensis L5 worms surviving in the central nervous system of human from inflammatory responses. Methods: Bioinformatics were used to analyse the structural characterisation of Acan-Gal-1; qRT-PCR and microinjection were performed to detect the expression patterns of Acan-gal-1; microinjection was performed to construct transgenic worms; oxidative stress assay and Oil Red O fat staining were used to determine the functions of Acan-Gal-1.Results: The results showed that Acan-Gal-1 was expressed ubiquitously and mainly localized in cuticle, and it was up-regulated in both L5 and adult worm. N2 worms expressing pCe-Acan-gal-1::Acan-gal-1::rfp, with lipid deposition reduced, were significantly resistant to oxidative stress. lec-1 mutant worms, with lipid deposition increased, showed susceptible to oxidative stress, and this phenotype could be rescued by expressing pCe-Acan-gal-1::Acan-gal-1::rfp. And fat-6;fat-7 double-mutant worms expressing pCe-Acan-gal-1::Acan-gal-1::rfp showed no significant changes in oxidative stress tolerance.Conclusion: In C. elegans worms, up-regulated Acan-Gal-1 plays a defensive role against damage due to oxidative stress for worm survival through reducing fat deposition. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-Gal-1 up-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

scholarly journals Alpha2-Adrenoblockers Regulate Development of Oxidative Stress and Cognitive Behaviour of Rats under Chronic Acoustic Stress Conditions

2021 ◽  
Vol 14 (6) ◽  
pp. 529
Author(s):  
Magdalina Melkonyan ◽  
Ashkhen Manukyan ◽  
Lilit Hunanyan ◽  
Artem Grigoryan ◽  
Hayk Harutyunyan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Noise Exposure ◽  
Male Rats ◽  
Behavioral Activity ◽  
Induced Stress ◽  
Y Maze ◽  
Cognitive Behaviour ◽  
The Central Nervous System ◽  
High Level ◽  
Environment Noise

Noise is a wide-spread stress factor in modern life produced by urbanization, traffic, and an industrialized environment. Noise stress causes dysfunction and neurotransmission impairment in the central nervous system, as well as changes in hormone levels. In this study, we have examined the level of α-Tocopherol (α-T) and malondialdehyde (MDA) in plasma and the erythrocytes’ membrane (EM), as well as the behavioral characteristics of a noise-induced stress model in rats. In addition, the modulating effect of α2-adrenoblockers, beditin, and mesedin on the aforementioned parameters has been investigated. For these purposes, albino male rats were divided into four groups: (1) untreated; (2) noise-exposed, (3) noise-exposed and beditin-treated (2 mg/kg, i.p.), and (4) noise-exposed and mesedin-treated (10 mg/kg, i.p.) animals. Noise-exposed groups were treated with 91dBA noise on 60 days with a daily duration of 8 h. Increased MDA and decreased α-T levels in plasma and EM were observed upon chronic high-level noise exposure. Locomotor and behavioral activity assessed with a Y-maze revealed disorientation and increased anxiety under chronic noise exposure. Prominently, α2-adrenoblockers alleviated both behavioral deficits and oxidative stress, providing evidence for the involvement of α2-adrenoceptor in the pathophysiology of noise-induced stress.

Oxidative Stress and Atherosclerosis: Its Relationship to Growth Factors, Thrombus Formation and Therapeutic Approaches

1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factors ◽  
Vessel Wall ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Vascular Lesion ◽  
Coagulation System ◽  
Therapeutic Approaches ◽  
Causative Relationship

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.

Physical exercise protects dynamic balance and motor coordination of rats treated with vincristine

2020 ◽  
Vol 19 (5) ◽  
pp. 336
Author(s):  
Luiza Minato Sagrillo ◽  
Viviane Nogueira De Zorzi ◽  
Luiz Fernando Freire Royes ◽  
Michele Rechia Fighera ◽  
Beatriz Da Silva Rosa Bonadiman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Locomotor Activity ◽  
Physical Exercise ◽  
Motor Coordination ◽  
Dynamic Balance ◽  
Exercise Group ◽  
Adult Rats ◽  
The Central Nervous System ◽  
Stress Damage ◽  
Training Protocol

Physical exercise has been shown to be an important modulator of the antioxidant system and neuroprotective in several diseases and treatments that affect the central nervous system. In this sense, the present study aimed to evaluate the effect of physical exercise in dynamic balance, motor coordination, exploratory locomotor activity and in the oxidative and immunological balance of rats treated with vincristine (VCR). For that, 40 adult rats were divided into two groups: exercise group (6 weeks of swimming, 1h/day, 5 days/week, with overload of 5% of body weight) and sedentary group. After training, rats were treated with 0.5 mg/kg of vincristine sulfate for two weeks or with the same dose of 0.9% NaCl. The behavioral tests were conducted 1 and 7 days after each dose of VCR. On day 15 we carried out the biochemical analyzes of the cerebellum. The physical exercise was able to protect against the loss of dynamic balance and motor coordination and, had effect per se in the exploratory locomotor activity, and neutralize oxidative stress, damage DNA and immune damage caused by VCR up to 15 days after the end of the training protocol. In conclusion, we observed that previous physical training protects of the damage motor induced by vincristine.Key-words: exercise, oxidative stress, neuroprotection, cerebellum.

Serum of 8-OHdG as a potential biomarker of oxidative DNA damage in workers exposed to harmful working environments

2020 ◽  
pp. 783-783
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Blood Serum ◽  
Oxidative Dna Damage ◽  
Working Environment ◽  
Working Environments ◽  
Potential Biomarker ◽  
High Level ◽  
Damage Marker

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

ВЛИЯНИЕ ОБЕДНЕННОГО ДЕЙТЕРИЕМ ПИТЬЕВОГО РАЦИОНА НА ФУНКЦИОНАЛЬНОЕ СОСТОЯНИЕ ЦЕНТРАЛЬНОЙ НЕРВНОЙ СИСТЕМЫ ЖИВОТНЫХ В УСЛОВИИ ГИПОКСИИ

2020 ◽  
Vol 65 (6) ◽  
pp. 1196-1202
Author(s):  
С.В. Козин ◽  
◽  
А.А. Кравцов ◽  
Э.И. Злищева ◽  
Л.В. Шурыгина ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Control Level ◽  
Learning Ability ◽  
Hypoxic Exposure ◽  
Amnestic Effect ◽  
Hypoxia With Hypercapnia ◽  
Antiamnestic Effect ◽  
The Central Nervous System ◽  
Deuterium Depleted Water

The effects of prolonged (42 days) addition of deuterium-depleted water into rat’s diet on the functional state of the central nervous system in normal conditions and under conditions of normobaric hypoxia with hypercapnia were studied. It was also established that the use of deuterium-depleted water both in normal conditions and after exposure to oxidative stress contributes to a significant reduction in the emotional anxiety of animals. Prolonged use of deuterium-depleted water before hypoxic exposure (amnestic effect) helps to maintain learning and memory at the control level, i.e. it has a pronounced protective antiamnestic effect. In normal conditions, deuterium-depleted water does not affect the learning ability of animals.

Resolution-Associated Molecular Patterns (RAMPs) as Endogenous Regulators of Glia Functions in Neuroinflammatory Disease

2020 ◽  
Vol 19 (7) ◽  
pp. 483-494
Author(s):  
Tyler J. Wenzel ◽  
Evan Kwong ◽  
Ekta Bajwa ◽  
Andis Klegeris
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Bioactive Lipids ◽  
Prothymosin Α ◽  
Neuroinflammatory Disease ◽  
Cellular Debris ◽  
Αb Crystallin ◽  
Endogenous Regulators ◽  
The Central Nervous System ◽  
Molecular Patterns

: Glial cells, including microglia and astrocytes, facilitate the survival and health of all cells within the Central Nervous System (CNS) by secreting a range of growth factors and contributing to tissue and synaptic remodeling. Microglia and astrocytes can also secrete cytotoxins in response to specific stimuli, such as exogenous Pathogen-Associated Molecular Patterns (PAMPs), or endogenous Damage-Associated Molecular Patterns (DAMPs). Excessive cytotoxic secretions can induce the death of neurons and contribute to the progression of neurodegenerative disorders, such as Alzheimer’s disease (AD). The transition between various activation states of glia, which include beneficial and detrimental modes, is regulated by endogenous molecules that include DAMPs, cytokines, neurotransmitters, and bioactive lipids, as well as a diverse group of mediators sometimes collectively referred to as Resolution-Associated Molecular Patterns (RAMPs). RAMPs are released by damaged or dying CNS cells into the extracellular space where they can induce signals in autocrine and paracrine fashions by interacting with glial cell receptors. While the complete range of their effects on glia has not been described yet, it is believed that their overall function is to inhibit adverse CNS inflammatory responses, facilitate tissue remodeling and cellular debris removal. This article summarizes the available evidence implicating the following RAMPs in CNS physiological processes and neurodegenerative diseases: cardiolipin (CL), prothymosin α (ProTα), binding immunoglobulin protein (BiP), heat shock protein (HSP) 10, HSP 27, and αB-crystallin. Studies on the molecular mechanisms engaged by RAMPs could identify novel glial targets for development of therapeutic agents that effectively slow down neuroinflammatory disorders including AD.

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