Modulation by Angelica Sinensis the expression of tumor necrosis factor α in radiation-induced damage of the lung

Objective To investigate the ability of Angelica Sinensis to affect the radiation-induced tumor necrosis factor α(TNF-α) release in the animal model, so as to find an effective method in reducing the lung toxicity after thoracic irradiation. Methods The chest of 72 C57BL/6 mice were exposed to either sham irradiation or single fraction of 12 ?Gy after having been randomized into 4 groups:1. 9 mice received neither irradiation nor Angelica Sinensis but received i.p injection of NS 20?ml/(kg·d)(NT group);2. 9 mice received Angelica Sinensis only but no irradiation though receiving i.p,NS(AS group);3. 27 mice received whole lung 12 ?Gy irradiation and i.p,NS without Angelica Sinensis (XRT group) and 4. 27 mice received both i.p,25% Angelica Sinensis 20?ml/(kg·d) and whole lung 12?Gy irradiation(AS/XRT group). The TNF-α mRNA expression in the lung tissue were quantified by 'real-time' quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Immunohistochemical detection method (Streptavidin-Peroxidase method) and positive cell counting were used for objective quantification of TNF-α protein expression. Results NT and AS group exhibited low level of TNF-α protein expression with positive cell counts between 8 and 17. And there was an significantly elevated level of TNF-α positive inflammatory cells in XRT group(P0.01). The number of the positive cells in AS/XRT group was between NT and AS group and XRT group with the difference between AS/XRT group and XRT group significant(P0.01). The results of 'real-time' quantitative RT-PCR showed that the relative mRNA expression of cytokine TNF-α in XRT group was significantly higher than the nonirradiated groups(P0.01).The lung tissue of the mice which were treated by Angelica Sinensis revealed only a minor radiation-mediated TNF-α response on mRNA level, but the statistical comparison of the TNF-a mRNA expressions between the XRT and AS/XRT groups was not significant(P=0.078),which was possibly due to the data variability and the relatively limited number of specimens available. Conclusions A significant radiation-induced increase of TNF-α in the lung tissue and the predominant localization of TNF-α in area of inflammatory cell infiltration suggests the involvement of cytokine in the pathogenesis of radiation-induced lung injury.