Modulation expression of tumor necrosis factor α in the radiation-induced lung injury by glycyrrhizic acid

Abstract

To evaluate the ability of glycyrrhizic acid (GLA) to reduce the tumor necrosis factor α (TNF-α), release on messenger ribonucleic acid (mRNA) and protein production in the lungs using GLA in response to irradiation were studied. The animals were divided into four groups: No treatment (NT group), GLA treatment only (GLA group), irradiation only (XRT group), and GLA treatment plus irradiation (GLA/XRT group). Rats were killed at different time points. Real-time reverse transcriptase polymerase chain reaction (RT-PCR) was used to evaluate the mRNA expression of TNF-α in the lungs (compared with non-irradiated lungs). An enzyme-linked immunosorbant assay (ELISA) assay was used to measure the TNF-α protein level. The TNF-α mRNA expression in the lungs of the XRT rats was clearly higher at all-time points compared to the NT rats. The TNF-α mRNA expression in the lungs of the GLA/XRT rats was lower at all-time points compared to the XRT rats. Release of the TNF-α on protein level in the lungs of the XRT rats increased at all-time points compared to the NT rats. In contrast to the XRT rats, the lungs of the GLA/XRT rats revealed a reduction on TNF-α protein level at 6 h after irradiation. This study has clearly showed the immediate down-regulation of the TNF-α mRNA and protein production in the lungs using GLA in response to irradiation.

Effect of captopril on radiation-induced TGF-β1 secretion in EA.Hy926 human umbilical vein endothelial cells

“…Whereas a significant increase in the expression of TNF-α mRNA was seen 3 months after radiation in A549 cells (Figure 2A), TNF-α mRNA levels in EA.Hy926 cells increased 4-fold one month after radiation, decreased between months 2 and 3, and increased again at month four post-radiation, compared with non-irradiated cells (Figure 2B). Our in vitro results may correlate with those obtained in animal models of radiation-induced lung damage, where TNF-α, primarily overexpressed in pulmonary epithelial cells, likely initiated with other cytokines the recruitment of macrophages and other inflammatory cells to inflammation sites very early post irradiation [16, 17]. Ionizing radiation activates various signaling pathways involved in the inflammatory process.…”

Biomarkers Associated with Radiation-Induced Lung Injury in Cancer Patients

“…for cascade responses [62] [63]. The enhanced plasma levels of TNF-α after radiation therapy are now well documented to be associated with early apoptosis and latent lung function impairment [64] [65] [66]. Despite the correlation between TNF-α and PR, however, there is still insufficient evidence as to whether TNF-α can be used as a predictor of RILT.…”

Promising Biomarkers of Radiation-Induced Lung Injury: A Review

“…TNF-α is the main initiator of the pro-inflammatory cascade by activating the expression of transcription factors, intercellular adhesion molecules, and numerous acute phase proteins. TNF-α also promotes fibroblast growth and collagen deposition [ 115 , 116 ]. Overproduction of TNF-α after irradiation has been well documented to be correlated with early cell apoptosis and latent lung function damage [ 117 ].…”