scholarly journals Effects of SLIRP on Sperm Motility and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Dan Shan ◽  
Samuel Kofi Arhin ◽  
Junzhao Zhao ◽  
Haitao Xi ◽  
Fan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Manganese Superoxide Dismutase ◽  
Mrna Level ◽  
Atp Content ◽  
Human Male ◽  
Manganese Superoxide ◽  
Polymerase Chain ◽  
And Oxidative Stress ◽  
Relative Mrna Expression

Background. Deficient spermatozoon motility is one of the main causes of male infertility. However, there are still no accurate and effective treatments in a clinical setting for male asthenospermia. Exploring the genes and mechanism of asthenospermia has become one of the hot topics in reproductive medicine. Our aim is to study the effect of SLRIP on human spermatozoon motility and oxidative stress. Methods. Sperm samples were collected including a normospermia group (60 cases) and an asthenospermia group (50 cases). SLIRP protein expression in spermatozoa was examined by western blotting, and relative mRNA expression of SLIRP in spermatozoa was quantified by reverse transcription polymerase chain reaction. Levels of reactive oxygen species (ROS), adenosine triphosphate (ATP) content, and the activity of manganese superoxide dismutase (MnSOD) in spermatozoa were also measured. Results. The mRNA level and protein expression of SLIRP in the asthenospermia group were significantly reduced compared with those in the normospermia group. The ROS active oxygen level in the asthenospermia group significantly increased; however, the ATP content decreased significantly as well as the activity of MnSOD. Conclusion. SLIRP regulates human male fertility, and SLIRP and sperm progressive motility are positively correlated. The expression of SLIRP is declined, oxidative damage is increased, and energy metabolism is decreased in spermatozoa of asthenospermia patients compared to normospermia participants.

scholarly journals Fucoxanthin Alleviates Oxidative Stress through Akt/Sirt1/FoxO3α Signaling to Inhibit HG-Induced Renal Fibrosis in GMCs

Marine Drugs ◽  
2019 ◽  
Vol 17 (12) ◽  
pp. 702 ◽  
Author(s):  
Guanyu Yang ◽  
Lin Jin ◽  
Dongxiao Zheng ◽  
Xiaoliang Tang ◽  
Junwei Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Manganese Superoxide Dismutase ◽  
Nuclear Transport ◽  
Reactive Oxygen Species Generation ◽  
Downstream Target ◽  
Forkhead Box ◽  
Manganese Superoxide ◽  
Lysine Deacetylase ◽  
Sirt1 Inhibitor ◽  
And Oxidative Stress

As one of the main marine carotenoids, fucoxanthin has strong antioxidant activity. FoxO3α, a member of the forkhead box O family of transcription factors, plays an important role in DN by regulating oxidative stress. The activity of FoxO3α is related to its phosphorylation and acetylation status, regulated by Akt and Sirt1, a lysine deacetylase. Our study aimed to investigate whether fucoxanthin could alleviate oxidative stress and fibrosis via FoxO3α in DN and whether Akt and Sirt1 were involved. We found that in GMCs cultured in HG, fucoxanthin treatment significantly reduced the expression of FN and collagen IV, as well as reactive oxygen species generation, suggesting that fucoxanthin is beneficial to alleviate both fibrosis and oxidative stress in DN. In addition, we found that fucoxanthin decreased the phosphorylation and acetylation level of FoxO3α, reversed the protein level of FoxO3α inhibited by HG, and then promoted the nuclear transport of FoxO3α. Besides, fucoxanthin promoted the expression of manganese superoxide dismutase, a downstream target of FoxO3α. Furthermore, we found that fucoxanthin reversed the activation of Akt and inhibition of Sirt1. However, the enhancement of fucoxanthin in FoxO3α expression and nuclear transport was significantly decreased by pretreatment with Akt activator SC79 or Sirt1 inhibitor EX527. In summary, our study explored fucoxanthin alleviated oxidative stress and fibrosis induced by HG through Akt/Sirt1/FoxO3α signaling in GMCs, suggesting fucoxanthin is a potential therapeutic strategy for DN.

Manganese Superoxide Dismutase and Oxidative Stress Modulation

2015 ◽  
pp. 87-130 ◽  
Author(s):  
Guilherme Bresciani ◽  
Ivana Beatrice Mânica da Cruz ◽  
Javier González-Gallego
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide ◽  
And Oxidative Stress

scholarly journals Genetic Polymorphisms of MnSOD Modify the Impacts of Environmental Melamine on Oxidative Stress and Early Kidney Injury in Calcium Urolithiasis Patients

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 152
Author(s):  
Chia-Chu Liu ◽  
Chia-Fang Wu ◽  
Yung-Chin Lee ◽  
Tsung-Yi Huang ◽  
Shih-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Manganese Superoxide Dismutase ◽  
Kidney Injury ◽  
Normal Function ◽  
Nucleotide Polymorphisms ◽  
Tubular Injury ◽  
Single Nucleotide ◽  
Manganese Superoxide ◽  
Calcium Urolithiasis ◽  
Renal Tubular

Environmental melamine exposure increases the risks of oxidative stress and early kidney injury. Manganese superoxide dismutase (MnSOD), glutathione peroxidase, and catalase can protect the kidneys against oxidative stress and maintain normal function. We evaluated whether their single-nucleotide polymorphisms (SNPs) could modify melamine’s effects. A total of 302 patients diagnosed with calcium urolithiasis were enrolled. All patients provided one-spot overnight urine samples to measure their melamine levels, urinary biomarkers of oxidative stress and renal tubular injury. Median values were used to dichotomize levels into high and low. Subjects carrying the T allele of rs4880 and high melamine levels had 3.60 times greater risk of high malondialdehyde levels than those carrying the C allele of rs4880 and low melamine levels after adjustment. Subjects carrying the G allele of rs5746136 and high melamine levels had 1.73 times greater risk of high N-Acetyl-β-d-glucosaminidase levels than those carrying the A allele of rs5746136 and low melamine levels. In conclusion, the SNPs of MnSOD, rs4880 and rs5746136, influence the risk of oxidative stress and renal tubular injury, respectively, in calcium urolithiasis patients. In the context of high urinary melamine levels, their effects on oxidative stress and renal tubular injury were further increased.

scholarly journals RNA-Seq Expression Analysis of Chronic Asthmatic Mice with Bu-Shen-Yi-Qi Formula Treatment and Prediction of Regulated Gene Targets of Anti-Airway Remodeling

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jie Cui ◽  
Zexi Lv ◽  
Fangzhou Teng ◽  
La Yi ◽  
Weifeng Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Network ◽  
Structural Changes ◽  
Airway Remodeling ◽  
Signal Pathways ◽  
Rna Seq ◽  
Critical Nodes ◽  
Differential Expression Genes ◽  
Polymerase Chain ◽  
And Oxidative Stress

Airway remodeling is one of the typical pathological characteristics of asthma, while the structural changes of the airways in asthma are complex, which impedes the development of novel asthma targeted therapy. Our previous study had shown that Bu-Shen-Yi-Qi formula (BSYQF) could ameliorate airway remodeling in chronic asthmatic mice by modulating airway inflammation and oxidative stress in the lung. In this study, we analysed the lung transcriptome of control mice and asthmatic mouse model with/without BSYQF treatment. Using RNA-sequencing (RNA-seq) analysis, we found that 264/1746 (15.1%) of transcripts showing abnormal expression in asthmatic mice were reverted back to completely or partially normal levels by BSYQF treatment. Additionally, based on previous results, we identified 21 differential expression genes (DEGs) with fold changes (FC) > (±) 2.0 related to inflammatory, oxidative stress, mitochondria, PI3K/AKT, and MAPK signal pathways which may play important roles in the mechanism of the anti-remodeling effect of BSYQF treatment. Through inputting 21 DEGs into the IPA database to construct a gene network, we inferred Adipoq, SPP1, and TNC which were located at critical nodes in the network may be key regulators of BSYQF's anti-remodeling effect. In addition, the quantitative real-time polymerase chain reaction (qRT-PCR) result for the selected four DEGs matched those of the RNA-seq analysis. Our results provide a preliminary clue to the molecular mechanism of the anti-remodeling effect of BSYQF in asthma.

Umbilical Cord Mesenchymal Stem Cell Exosomes Alleviate the Progression of Kidney Failure by Modulating Inflammatory Responses and Oxidative Stress in an Ischemia-Reperfusion Mice Model

2021 ◽  
Vol 17 (9) ◽  
pp. 1874-1881
Author(s):  
Yanqiang Zhang ◽  
Chongjuan Wang ◽  
Zhuxiao Bai ◽  
Peng Li
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Renal Failure ◽  
Stem Cell ◽  
Protein Expression ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Protein Expression Level ◽  
M1 Macrophages ◽  
And Oxidative Stress

The efficacy of stem cells for the treatment of renal failure is widely recognized; however, an excessive volume of stem cells can block the capillaries; thus, the potential risks should not be ignored. Stem cell exosomes are secretory extracellular vesicles with a size of 30–150 nm, which have similar functions to stem cells but are much smaller in size. This study aims to investigate the role of human umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes in the treatment of renal failure caused by ischemia-reperfusion. Fifty 8-week-old female C57 mice underwent bilateral renal ischemia-reperfusion surgery for 30 minutes. After 4 weeks, the treated group received UCMSCs-derived exosomes treatment, and the control group was solely injected with the same amount of PBS. At the age of 16 weeks, the kidney function, kidney damage, inflammatory responses and oxidative stress were measured. Moreover, the effect of UCMSCs-derived exosomes on the phenotype of M1 macrophages was also tested. The results showed that UCMSCsderived exosomes significantly reduced the levels of blood urea nitrogen (BUN), serum creatinine (SCR), and urinary albumin and creatinine (ACR) and 8-isoprostane. UCMSCs-derived exosomes also improved the atrophy of the kidney and glomerulus, decreased kidney pro-inflammatory factors expression (mRNA of II-1β, II-6, Tnf-α, and Mcp-1) and oxidative stress (malondialdehyde), and increased glutathione level. However, F4/80 immunohistochemistry did not show significant differences between the two groups. In systemic inflammation measurement, UCMSCs-derived exosomes decreased proinflammatory factors TNF-α, IL-6, and IL-1β levels, and increased anti-inflammatory factor IL-10 level. In vitro experiments showed that UCMSCs-derived exosomes decreased the protein expression level of TNF-α and increased the protein expression level of IL-10 in M1 macrophages. UCMSCs-derived exosomes reduce kidney inflammation and oxidative stress by improving systemic inflammation, and thus reduce kidney damage and improve kidney function. This study shows the potential application value of exosomes in the treatment of renal failure.

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