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

AI Article Synopsis

  • This study investigated how glycyrrhizic acid (GLA) affects the production of TNF-α, a protein linked to inflammation, in the lungs of rats exposed to radiation.
  • The rats were divided into four groups: one received no treatment, one received only GLA, one was irradiated, and one received both GLA and irradiation.
  • Results showed that GLA significantly lowered TNF-α levels in the lungs after irradiation, indicating its potential as an anti-inflammatory agent in this context.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478651PMC
http://dx.doi.org/10.4103/0971-6203.158689DOI Listing

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