Granulocyte colony-stimulating factor (G-CSF) production by astrocytoma cells and its effect on tumor growth

1996 ◽  
Vol 27 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Tetsuro Kikuchi ◽  
Shigehiro Nakahara ◽  
Toshiaki Abe
Keyword(s):  
Tumor Growth ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Astrocytoma Cells ◽  
Stimulating Factor ◽  
Csf Production ◽  
Factor G

scholarly journals Analysis of Serum Granulocyte-Colony Stimulating Factor(G-CSF) and G-CSF Production in Lung Cancer with Leukocytosis.

Haigan ◽  
1997 ◽  
Vol 37 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Ikuma Kasuga ◽  
Yuichi Ichinose ◽  
Makoto Yonemaru ◽  
Harubumi Katoh ◽  
Keisuke Toyama
Keyword(s):  
Lung Cancer ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Csf Production ◽  
Factor G

scholarly journals Can granulocyte colony stimulating factor (G-CSF) ameliorate acetaminophen-induced hepatotoxicity?

2021 ◽  
pp. 096032712110085
Author(s):  
EA Ahmed ◽  
AM Abd-Eldayem ◽  
E Ahmed
Keyword(s):  
Liver Damage ◽  
Liver Toxicity ◽  
Serum Levels ◽  
Hepatic Tissue ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Oxidative Markers ◽  
Stimulating Factor ◽  
New Strategies ◽  
Factor G

Acetaminophen (APAP) is often used as an antipyretic and analgesic agent. Overdose hepatotoxicity, which often results in liver cell failure and liver transplantation, is a severe complication of APAP usage. To save the liver and save lives from acute liver damage caused by APAP, the search for new strategies for liver defense is important. Wistar rats have been used for the induction of APAP hepatotoxicity. Elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were evaluated for liver toxicity. In addition, the levels of hepatic tissue oxidative markers such as malondialdehyde (MDA), nitric oxide (NO) increased while glutathione (GSH) was depleted and catalase (CAT) activity was curtailed. The biochemical findings were consistent with the changes in histology that suggested liver damage and inflammation. Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high. After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity. Treatment with N-AC and G-CSF after administration of APAP has also attenuated inflammation and hepatocytes necrosis. The results of this study showed that G-CSF could be viewed as an alternative hepatoprotective agent against APAP-induced acute liver injury compared to N-AC.

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