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.

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 Exposure of cigarette smoke aggravates noise induced kidney damage

2020 ◽  
Vol 10 (2) ◽  
pp. e12-e12
Author(s):  
Jamshid Alizadeh ◽  
Zohre Jaffarzadeh ◽  
Kambiz Ahmadi Angali ◽  
Massumeh Ahmadizadeh
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Cigarette Smoke ◽  
Noise Exposure ◽  
Health Hazard ◽  
Male Rats ◽  
Sodium Pentobarbital ◽  
Biochemical Tests ◽  
Sound Exposure ◽  
The Impact

Introduction: Noise is defined as an interfering and unwanted sound. Exposure to noise induces health problems in humans and animals. Cigarette smoke (CS) has also been known to cause serious problems in health hazard and leads to many kinds of diseases. However, the effects of these agents on the kidney are poorly studied. Objectives: The current study purposes to investigate the impact of noise and/or CS on rat’s kidney Materials and Methods: Four groups of six Wistar adult male rats were used. They randomly were divided into four groups of rats. The first group was used as control. The second group was exposed to noise. The third group was exposed to cigarette smoking and the fourth group was exposed to both noise and CS. The experiments were repeated for two weeks (five days per week). Twenty-four hours after last exposure, the animals were killed by sodium pentobarbital overdose. Renal function was evaluated by the determination of blood urea nitrogen (BUN) and creatinine levels. Oxidative stress was estimated by glutathione (GSH) and malondialdehyde (MDA) assays. Results: The concentrations of BUN and creatinine remarkably raised (P ≤ 0.05) in all groups compared to those in control rats. However, elevations of the biochemical tests were more predominant in rats exposed to combined noise and CS. Elevation of MDA was observed in all exposed rats, while it was more pronounced in the animals exposed to the combined noise and CS when compared to control, CS or noise exposure rats alone. The level of GSH decreased in all exposed groups. It was more obvious in rats exposed to the combined noise and CS when compared to those of control and exposure rats to noise or CS separately. Conclusion: Exposure to noise or CS impaired renal function. Generation of oxidative stress at least in part may be responsible for their nephrotoxicity. Our findings demonstrated CS aggravated noise induced impairment of renal function.

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 Transcriptional re-programming in rat central nervous system two weeks after burn trauma: the impact of nephrilin treatment on the expression of oxidative stress-related genes

2020 ◽  
Vol 6 ◽  
pp. 205951312093944
Author(s):  
Desmond D Mascarenhas
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disease ◽  
Pcr Amplification ◽  
Male Rats ◽  
Burn Trauma ◽  
The Central Nervous System ◽  
Key Genes ◽  
The Impact

Introduction: Survivors of severe burns suffer lifetime neuroinflammatory consequences manifested by higher incidence of major depression and neurodegenerative disease. In a scald model, nephrilin peptide has previously been shown to protect rats from loss of lean body mass, kidney function and glycaemic control, complications that have also been shown to endure in burn patient populations. Nephrilin’s mechanism of action has been suggested to involve protection from excessive oxidative stress. Methods: Using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) amplification of transcripts in total RNA extracted from dorsal root ganglia of male rats 14 days after exposure to thermal insult, we query the relative levels of expression of 34 genes believed to be associated with oxidative stress biology in the central nervous system (CNS). We use these data to explore the central role of oxidative stress in astrogliosis, immunosuppression and mitochondrial homeostasis. Results and Discussion: Rats that received nephrilin treatment (4 mg/kg by subcutaneous bolus injection once daily for seven days after scald injury) showed significantly reduced elevations in gene expression of some key genes such as NOX2, GFAP, AQP4 and RAC1, but not of others such as NOX4, STEAP4, ARG1 and CCL2. Conclusion: The implications of these data with reference to nephrilin’s potential clinical utility for mitigating the enduring effects of burn trauma on the CNS are discussed. Nephrilin reduces the expression of some genes implicated in neurodegeneration after burn insult. Lay Summary Nephrilin peptide is a novel treatment for short- and long-term systemic effects of burn trauma. This study measures the capability of nephrilin to address post-traumatic neurodegenerative disease by looking at the expression of genes in the central nervous system, in a rat scald model. Nephrilin appears to have beneficial effects by reducing the expression of some key genes known to be relevant in neurodegenerative processes, but not others.

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 Effect of long-term emotional-painful stress on the leukocyte composition of blood in rats with different levels of excitability of the nervous system

2020 ◽  
Author(s):  
Irina G. Shalaginova ◽  
Vera Sheremet ◽  
Diana A. Khlebaeva ◽  
Alexander I. Vaido ◽  
Natalia A. Dyuzhikova
Keyword(s):  
Nervous System ◽  
Chronic Stress ◽  
Male Rats ◽  
High Threshold ◽  
The Central Nervous System ◽  
Stress States ◽  
High Level ◽  
Genetically Determined ◽  
Immune Dysfunctions

AbstractPost-stress states in animals and humans are accompanied by the development of neuro- and peripheral inflammation. The mechanisms of such immune dysfunctions, their contribution to the pathogenesis of stress-related diseases, as well as the dependence of the intensity of poststress inflammation on genetically determined features of the nervous system, have not been clarified.Aim: to assess the dynamics of the development of poststress inflammation depending on the genetically determined level of excitability of the nervous system in rats.Materials and methods. The study was carried out on male rats of two lines, selected by the threshold of excitability of the nervous system-the line HT (high threshold of excitability) and LT (low threshold of excitability). As a model of chronic stress, the Protocol of long-term emotional and pain exposure according to Hecht was used. To investigate the dynamics of changes in the leukocyte formula, three time points were selected: 24 hours, 7 days and 24 days after the stressor. Morphological analysis of blood was carried out to determine the leukogram, for which the leukocytes were counted in a blood smear stained by Romanovsky-Gimza.Results. Chronic stress leads to an increase in the leukocyte shift index only in the experimental group of highly excitable rats of the LT line compared with control animals of the same line. The significance of the differences is confirmed on day 7 after the end of the stressor. No interline differences in neutrophil/lymphocyte ratios were found in intact animals of LT and HT lines.Conclusion. In rats with a genetically determined high level of excitability of the nervous system, post-stressor systemic inflammation appears 7 days after the end of the stressor. Animals with a low level of excitability of the nervous system had no signs of post-stress inflammation throughout the observations. The article discusses the possible mechanisms of detected immune dysfunctions in animals due to high excitability of the central nervous system.

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.

Effect of Turmeric and Ginger on Lipid Profile in Male Rats Exposed to Oxidative Stress

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Control Group ◽  
Very Low Density Lipoprotein ◽  
Low Density

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.

PROTECTIVE EFFECT OF SOME SALTS 2-AMINOETHANESULFONIC ACID IN AN EXPERIMENTAL MODEL OF DEGENERATIVE SPINAL CORD INJURY

2020 ◽  
pp. 41-47
Author(s):  
Semeleva E.V. ◽  
Blinova E.V. ◽  
Zaborovsky A.V. ◽  
Vasilkina O.V. ◽  
Shukurov A.S.
Keyword(s):  
Spinal Cord ◽  
Morphological Changes ◽  
Male Rats ◽  
Zinc Salt ◽  
Control Group ◽  
Morphological Studies ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Acid Compound ◽  
Lateral Sclerosis

In this work, we studied the pharmacological activity of zinc and magnesium salts of 2-aminoethanesulfonic acid in white non-linear male rats with amyotrophic lateral sclerosis, which was modeled by neurotoxicantsimplication into the pelvic part of spinal cord. After the reproduction of the pathology in animals, the indices of motor activity were recorded in the Rotarod test, and morphological studies of spinal cord sections stained according to Nisl in the Belshovsky modification were carried out. It was shown that the magnesium salt of 2-aminoethanesulfonic acid (compound LHT-317) to a greater extent reduces the development of motor disorders in experimental animals compared with the control group on the 4th day of observation. The course of intravenous administration of the studied compounds of 2-aminoethanesulfonic acid did not inhibit morphological changes in the spinal cord that develop in degenerative-dystrophic pathology of the central nervous system: connections. Moreover, if, against the background of treatment with zinc salt, the total area of motor zones in animals of the experimental group exceeded that of control rats, then the number of motoneurons did not differ from the control.

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