scholarly journals Metabolomics reveals potential plateau adaptability by regulating inflammatory response and oxidative stress-related metabolism and energy metabolism pathways in yak

Author(s):  
Huang Meizhou ◽  
Zhang Xin ◽  
Yan Wenjun ◽  
Liu Jingjing ◽  
Wang Hui
Inflammation ◽  
2014 ◽  
Author(s):  
Thiago Henrique Costa Marques ◽  
Maria Leonildes Boavista Gomes Cast Marques ◽  
Jand-Venes R. Medeiros ◽  
Renan Oliveira Silva ◽  
André Luiz dos Reis Barbosa ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.


2018 ◽  
Vol 310 (9) ◽  
pp. 759-767 ◽  
Author(s):  
Tuğba Falay Gur ◽  
Aslı Vefa Erdemir ◽  
Mehmet Salih Gurel ◽  
Abdurrahim Kocyigit ◽  
Eray Metin Guler ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Qianru Chi ◽  
Dongxu Wang ◽  
Xueyuan Hu ◽  
Shiping Li ◽  
Shu Li

Hydrogen sulfide (H2S) is one of the main pollutants in the atmosphere, which is a serious threat to human health. The decomposition of sulfur-containing organics in chicken houses could produce a large amount of H2S, thereby damaging poultry health. In this study, one-day-old broilers were selected and exposed to 4 or 20 ppm of H2S gas (0-3 weeks: 4±0.5 ppm, 4-6 weeks: 20±0.5 ppm). The spleen samples were collected immediately after the chickens were euthanized at 2, 4, and 6 weeks. The histopathological and ultrastructural observations showed obvious necrosis characteristics of H2S-exposed spleens. H2S exposure suppressed GSH, CAT, T-AOC, and SOD activities; increased NO, H2O2, and MDA content and iNOS activity; and induced oxidative stress. ATPase activities and the expressions of energy metabolism-related genes were significantly decreased. Also, the expressions of related necroptosis (RIPK1, RIPK3, MLKL, TAK1, TAB2, and TAB3) were significantly increased, and the MAPK pathway was activated. Besides, H2S exposure activated the NF-κB classical pathway and induced TNF-α and IL-1β release. Taken together, we conclude that H2S exposure induces oxidative stress and energy metabolism dysfunction; evokes necroptosis; activates the MAPK pathway, eventually triggering the NF-κB pathway; and promotes inflammatory response in chicken spleens.


Author(s):  
Alaaeldin Ahmed Hamza ◽  
Mona Gamel Mohamed ◽  
Fawzy Mohamed Lashin ◽  
Amr Amin

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