scholarly journals In vitro suppression of serum elastase-inhibitory capacity by reactive oxygen species generated by phagocytosing polymorphonuclear leukocytes.

1979 ◽  
Vol 63 (4) ◽  
pp. 793-797 ◽  
Author(s):  
H Carp ◽  
A Janoff
1998 ◽  
Vol 11 (3) ◽  
pp. 155-162 ◽  
Author(s):  
M. Dušková ◽  
L. Dušek ◽  
M. Čìž ◽  
A. Lojek ◽  
H. Slavíková

The effect of azathioprine, cyclosporine A and FK 506 on the production of reactive oxygen species by polymorphonuclear leukocytes (Iuminol-dependent chemiluminescence) and on the blast transformation of lymphocytes ([3H]thymidine incorporation) was studied in dose-response experiments under in vitro conditions. Although there were no significant effects of immunosuppressives on non-stimulated blast transformation, FK 506 and cyclosporine A significantly inhibited the blast transformation stimulated by concanavaline A and protein A and the effects made it possible to build 2nd-order polynomial dose-response models. Azathioprine was found to be a relatively weak inhibitor of [3H]thymidine incorporation in lymphocytes (76% of control value). Spontaneous production of reactive oxygen species by polymorphonuclear leukocytes was significantly inhibited, particularly by FK 506 (1–100 ng.ml−1) in comparison to the control value, while there was no effect of the immunosuppressives on this system activated either by starch grains or zymosan. Only the highest applied concentrations of azathioprine (100 ng.ml−1) and cyclosporine A (1000 ng.ml−1) led to a significant decline in spontaneous phagocytosis. The direct effect of immunosuppressives on activated production of reactive oxygen species by neutrophiles was not proved.


2007 ◽  
Vol 140 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Wilhelmina M.U. van Grevenstein ◽  
Arend G.J. Aalbers ◽  
Sander ten Raa ◽  
Wim Sluiter ◽  
Leo J. Hofland ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 388
Author(s):  
Xiao Dan Hui ◽  
Gang Wu ◽  
Duo Han ◽  
Xi Gong ◽  
Xi Yang Wu ◽  
...  

In this study, blueberry and blackcurrant powder were chosen as the phenolic-rich enrichments for oat bran. A Rapid Visco Analyser was used to form blueberry and blackcurrant enriched oat pastes. An in vitro digestion process evaluated the changes of phenolic compounds and the in vitro antioxidant potential of extracts of pastes. The anthocyanidin profiles in the extracts were characterised by the pH differential method. The results showed that blueberry and blackcurrant powder significantly increased the content of phenolic compounds and the in vitro antioxidant capacity of pastes, while the total flavonoid content decreased after digestion compared to the undigested samples. Strong correlations between these bioactive compounds and antioxidant values were observed. Lipopolysaccharide-stimulated RAW264.7 macrophages were used to investigate the intracellular antioxidant activity of the extracts from the digested oat bran paste with 25% enrichment of blueberry or blackcurrant powder. The results indicated that the extracts of digested pastes prevented the macrophages from experiencing lipopolysaccharide (LPS)-stimulated intracellular reactive oxygen species accumulation, mainly by the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) signalling pathway. These findings suggest that the bioactive ingredients from blueberry and blackcurrant powder enhanced the in vitro and intracellular antioxidant capacity of oat bran pastes, and these enriched pastes have the potential to be utilised in the development of the functional foods.


2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhuochao Liu ◽  
Hongyi Wang ◽  
Chuanzhen Hu ◽  
Chuanlong Wu ◽  
Jun Wang ◽  
...  

AbstractIn this study, we identified the multifaceted effects of atezolizumab, a specific monoclonal antibody against PD-L1, in tumor suppression except for restoring antitumor immunity, and investigated the promising ways to improve its efficacy. Atezolizumab could inhibit the proliferation and induce immune-independent apoptosis of osteosarcoma cells. With further exploration, we found that atezolizumab could impair mitochondria of osteosarcoma cells, resulting in increased release of reactive oxygen species and cytochrome-c, eventually leading to mitochondrial-related apoptosis via activating JNK pathway. Nevertheless, the excessive release of reactive oxygen species also activated the protective autophagy of osteosarcoma cells. Therefore, when we combined atezolizumab with autophagy inhibitors, the cytotoxic effect of atezolizumab on osteosarcoma cells was significantly enhanced in vitro. Further in vivo experiments also confirmed that atezolizumab combined with chloroquine achieved the most significant antitumor effect. Taken together, our study indicates that atezolizumab can induce mitochondrial-related apoptosis and protective autophagy independently of the immune system, and targeting autophagy is a promising combinatorial approach to amplify its cytotoxicity.


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