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.

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

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 Hippocampal Lipocalin 2 Is Associated With Neuroinflammation and Iron-Related Oxidative Stress in ob/ob Mice

2020 ◽  
Vol 79 (5) ◽  
pp. 530-541 ◽  
Author(s):  
Zhen Jin ◽  
Kyung Eun Kim ◽  
Hyun Joo Shin ◽  
Eun Ae Jeong ◽  
Kyung-Ah Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Structural Changes ◽  
Brain Injuries ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Lipocalin 2 ◽  
Rna Seq ◽  
Iron Binding Protein ◽  
Metalloproteinase 9

Abstract Obesity causes brain injuries with inflammatory and structural changes, leading to neurodegeneration. Although increased circulating lipocalin 2 (LCN2) level has been implicated in neurodegenerative diseases, the precise mechanism of neurodegeneration in obesity is not clear. Here, we investigated whether LCN2-mediated signaling promotes neurodegeneration in the hippocampus of leptin-deficient ob/ob mice, which are characterized by obesity, insulin resistance, systemic inflammation, and neuroinflammation. In particular, there was significant upregulation of both LCN2 and matrix metalloproteinase 9 levels from serum and hippocampus in ob/ob mice. Using RNA-seq analysis, we found that neurodegeneration- sortilin-related receptor 1 (Sorl1) and brain-derived neurotrophic factor (Bdnf) genes were significantly reduced in the hippocampus of ob/ob mice. We additionally found that the endosome-related WD repeat and FYVE-domain-containing 1 (Wdfy1) gene were upregulated in ob/ob mice. In particular, iron overload-related mitochondrial ferritin and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) proteins were increased in the hippocampus of ob/ob. Thus, these findings indicate that iron-binding protein LCN2-mediated oxidative stress promotes neurodegeneration in ob/ob mice.

scholarly journals Improvement of lung ischemia–reperfusion injury by inhibition of microRNA-155 via reductions in neuroinflammation and oxidative stress of vagal afferent nerve

2020 ◽  
Vol 10 (2) ◽  
pp. 204589402092212
Author(s):  
Yan Zhou ◽  
Lianjie Zhang ◽  
Jingjing Guan ◽  
Xin Yin
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Proinflammatory Cytokines ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Signal Pathways ◽  
Afferent Nerves ◽  
Tnf Α ◽  
Vagal Afferent ◽  
And Oxidative Stress

Lung ischemia–reperfusion injury (LIRI) is a common clinical concern. As the injury occurs, the pulmonary afferent nerves play a key role in regulating respiratory functions under pathophysiological conditions. The present study was to examine the effects of inhibiting microRNA-155 on the levels of proinflammatory cytokines and products of oxidative stress in the pulmonary vagal afferent nerves and the commissural nucleus of the solitary tract (cNTS) after LIRI. A rat model of LIRI was used. ELISA method was employed to examine proinflammatory cytokines, namely, IL-1β, IL-6 and TNF-α; and key biomarkers of oxidative stress, 8-isoprostaglandin F2α (8-iso PGF2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). In results, in the process of LIRI, the levels of microRNA-155 were amplified in the vagal afferent nerves and cNTS, and this was accompanied with increases of IL-1β, IL-6 and TNF-α; and 8-iso PGF2α and 8-OHdG. Application of microRNA-155 inhibitor, but not its scramble, attenuated the elevation of proinflammatory cytokines and amplification of 8-iso PGF2α and 8-OHdG in those nerve tissues. In conclusion, we observed the abnormalities in the pulmonary afferent pathways at the levels of the peripheral nerves and brainstem, which is likely to affect respiratory functions as LIRI occurs. Our data suggest that blocking microRNA-155 signal pathways plays a beneficial role in regulating LIRI via inhibiting responses of neuroinflammation and oxidative stress signal pathways to LIRI.

scholarly journals Expression profiles of genes associated with inflammatory responses and oxidative stress in lung after heat stroke

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Zhaoyu Liu ◽  
Jitao Chen ◽  
La Hu ◽  
Ming Li ◽  
Min Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Lung Injury ◽  
Heat Stroke ◽  
Signal Pathways ◽  
Important Place ◽  
Network Analyses ◽  
Qrt Pcr ◽  
Cell Enrichment ◽  
And Oxidative Stress

Abstract Background: Heat stroke (HS) is a physically dysfunctional illness caused by hyperthermia. Lung, as the important place for gas-exchange and heat-dissipation organ, is often first to be injured. Lung injury caused by HS impairs the ventilation function of lung, which will subsequently cause damage to other tissues and organs. Nevertheless, the specific mechanism of lung injury in heat stroke is still unknown. Methods: Rat lung tissues from controls or HS models were harvested. The gene expression profile was identified by high-throughput sequencing. DEGs were calculated using R and validated by qRT-PCR. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and cell-enrichment were performed using differential expression genes (DEGs). Finally, lung histopathology was accessed by H&E staining. Results: About 471 genes were identified to be DEGs, of which 257 genes were up-regulated, and 214 genes were down-regulated. The most up-regulated and down-regulated DEGs were validated by qRT-PCR, which confirmed the tendency of expression. GO, KEGG, and protein–protein interaction (PPI)-network analyses disclosed DEGs were significantly enriched in leukocyte migration, response to lipopolysaccharide, NIK/NF-kappaB signaling, response to reactive oxygen species, response to heat, and the hub genes were Tnf, Il1b, Cxcl2, Ccl2, Mmp9, Timp1, Hmox1, Serpine1, Mmp8 and Csf1, most of which were closely related to inflammagenesis and oxidative stress. Finally, cell-enrichment analysis and histopathologic analysis showed Monocytes, Megakaryotyes, and Macrophages were enriched in response to heat stress. Conclusions: The present study identified key genes, signal pathways and infiltrated-cell types in lung after heat stress, which will deepen our understanding of transcriptional response to heat stress, and might provide new ideas for the treatment of HS.

scholarly journals Light Irradiation Coupled with Exogenous Metal Ions to Enhance Exopolysaccharide Synthesis from Agaricus sinodeliciosus ZJU-TP-08 in Liquid Fermentation

2021 ◽  
Vol 7 (11) ◽  
pp. 992
Author(s):  
Hongyun Lu ◽  
Siyu Liu ◽  
Shengliang Zhang ◽  
Qihe Chen
Keyword(s):  
Oxidative Stress ◽  
Metal Ions ◽  
Blue Light ◽  
Light Treatment ◽  
Light Shift ◽  
Rna Seq ◽  
Gene Expressions ◽  
Shift Strategy ◽  
And Oxidative Stress ◽  
Exopolysaccharides Production

To promote Agaricus sinodeliciosus var. Chaidam ZJU-TP-08 growth and metabolites accumulation, a novel integrated strategy was developed by adopting high levels of metal ions coupled with light treatment. The results revealed that yellow and blue light could significantly promote biomass and exopolysaccharides production, respectively. Furthermore, the yellow–blue light shift strategy could stimulate exopolysaccharides formation. Ca2+ ions coupled with blue light mostly promoted exopolysaccharides production related to oxidative stress, which was 42.00% and 58.26% higher than that of Ca2+ ions coupled with the non-light and dark cultivation without Ca2+ ions in 5-L bioreactor. RNA-seq was performed to uncover the underlined molecular mechanism regulated by light-induced gene expressions in exopolysaccharides biosynthesis and oxidative stress. The findings of this work provide valuable insights into adopting metal ions coupled with the light-assisted method for the macrofungus submerged fermentation for exopolysaccharides production.

Ampelopsin Improves Cognitive Impairment in Alzheimer’s Disease and Effects of Inflammatory Cytokines and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 17 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Yan Wang ◽  
Wei Lv ◽  
Yueyang Li ◽  
Dandan Liu ◽  
Xiuting He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Working Memory ◽  
Learning Performance ◽  
Signal Pathways ◽  
Tnf Α ◽  
Cognitive Deficiency ◽  
Improved Learning ◽  
And Oxidative Stress

Background: Neuroinflammation and oxidative stress have significant effects on cognitive deficiency in the pathophysiological development of Alzheimer’s disease (AD). In the present study, we studied the influences of Ampelopsin (AMP) on proinflammatory cytokines (PICs, IL-1β, IL-6 and TNF-α), and products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, a product of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, a key biomarker of protein oxidation) in the hippocampus using a rat model of AD. Methods: ELISA was used to examine PICs and oxidative stress production; and western blotting to examine NADPH oxidase (NOXs). The Spatial working memory tests and Morris water maze were utilized to assess cognitive functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α as well as 8-iso PGF2α and 8-OHdG in the hippocampus of AD rats. AMP attenuated upregulation of PICs and oxidative stress production. AMP also inhibited NOX4 in the AD rat hippocampus. Notably, AMP mostly improved learning performance in AD rat and this was linked to signal pathways of PIC and oxidative stress. Conclusion: AMP plays a significant role in improving the memory deficiency in AD rats via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that AMP is likely to prospect in preventing and relieving development of the cognitive dysfunctions in AD as a complementary alternative intervention.

scholarly journals Structural changes in dermal collagen and oxidative stress levels in the skin of Japanese overweight males

2014 ◽  
Vol 36 (5) ◽  
pp. 477-484 ◽  
Author(s):  
M. Matsumoto ◽  
A. Ibuki ◽  
T. Minematsu ◽  
J. Sugama ◽  
M. Horii ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Structural Changes ◽  
Stress Levels ◽  
Dermal Collagen ◽  
And Oxidative Stress
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