凉血活血中药治疗放射性肺损伤的实验研究

作者	单位
杨明会	解放军总医院中医研究所
窦永起	解放军总医院中医研究所
臧倩	解放军总医院中医研究所
冯林春	解放军总医院放疗科
刘毅	解放军总医院中医研究所

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Objective To investigate the effect of blood-cooling and promoting drugs (BCPD) on the dynamic changes of collagens and the expressions of interleukin-6 (IL-6)and transforming growth factor beta (TGF-β) in lung tissue of rats with radiation-induced lung injury (RILI) to explore the effects and action mechanism of BCPD in preventing and treating RILI. Methods One hundred and sixty Wistar female rats were randomly divided into the radiation group, the treatment group, the blank control group and the drug control group. The rats in the first two groups received right hemithoracic fractionated radiation, and those in the treatment group were given BCPD. Rats in the other two groups were not irradiated and BCPD was given to rats in the drug control group. The rats were sacrificed in batches (8 of each group in every batch) at the 3rd, 5th, 8th, 12th and 26th week of the experimental period, and their lung was taken for observing the dynamic changes and distribution of collagen and the expressions of IL-6 and TGF-β with HE staining, picrosirius red staining and immunohistochemical staining respectively. Results The fibroblast proliferated obviously from the 3rd week after the first radiation in the radiation group, and the type Ⅰ collagen and the proportion of type Ⅰ and Ⅲ collagen were significantly elevated along the time going and the radiation dose increasing, became significantly higher than those in the treatment group at all the time points (P<0.01). In the radiation group the expression of IL-6 and TGF-β reached their peaks at the 8th and 12th week, respectively, and the levels was significantly lower in the treatment than that in the radiation group at any detecting time points (P<0.01). Conclusion BCPD applied in the early stage of radiation can suppress the inflammatory and fibrogenic cytokine expressions, inhibit the synthesis of collagens and adjust the proportion of type Ⅰ and Ⅲ collagen, so as to relieve the early-stage inflammatory reaction and the anaphase lung fibrosis in RILI rats.

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