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首页> 外文期刊>Journal of Radiation Research: Official Organ of the Japan Radiation Research Society >Protective effects of ulinastatin and methylprednisolone against radiation-induced lung injury in mice
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Protective effects of ulinastatin and methylprednisolone against radiation-induced lung injury in mice

机译:乌司他丁和甲基强的松龙对辐射诱发的小鼠肺损伤的保护作用

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The effectiveness of ulinastatin and methylprednisolone in treating pathological changes in mice with radiation-induced lung injury (RILI) was evaluated. Forty C57BL/6 female mice received whole-chest radiation (1.5 Gy/min for 12 min) and were randomly allocated into Group R (single radiation, n = 10), Group U (ulinastatin treatment, = 10), Group M (methylprednisolone treatment, = 10), or Group UM (ulinastatin and methylprednisolone treatment, = 10). Another 10 untreated mice served as controls (Group C). Pathological changes in lung tissue, pulmonary interstitial area density (PIAD) and expression levels of transforming growth factor beta 1 (TGF-beta 1) and tumor necrosis factor alpha (TNF-alpha) in lung tissue, serum and bronchoalveolar lavage fluid were determined. Alleviation of pathological changes in lung tissue was observed in Groups U, M and UM. Treatment with ulinastatin, methylprednisolone or both effectively delayed the development of fibrosis at 12 weeks after radiation. Ulinastatin, methylprednisolone or both could alleviate the radiation-induced increase in the PIAD (P < 0.05 or P < 0.01). Treatment with ulinastatin, methylprednisolone or both significantly reduced the expression of TNF-alpha, but not TGF-beta 1, at 9 weeks after radiation compared with Group R (P < 0.01). Ulinastatin and/or methylprednisolone effectively decreased the level of TNF-alpha in lung tissue after RILI and inhibited both the inflammatory response and the development of fibrosis.
机译:评估了乌司他丁和甲基强的松龙在治疗辐射诱发性肺损伤(RILI)小鼠病理变化中的有效性。 40只C57BL / 6雌性小鼠接受全胸照射(1.5 Gy / min,持续12分钟),并随机分为R组(单次放射,n = 10),U组(乌司他丁治疗,= 10),M组(甲基泼尼松龙)治疗组= 10)或UM组(乌司他丁和甲基泼尼松龙治疗组= 10)。另外10只未治疗的小鼠用作对照(C组)。测定肺组织,血清和支气管肺泡灌洗液中肺组织的病理学变化,肺间质区域密度(PIAD)以及转化生长因子β1(TGF-beta 1)和肿瘤坏死因子α(TNF-alpha)的表达水平。在U,M和UM组中观察到肺组织病理变化的减轻。乌拉司他丁,甲基强的松龙或两者联合治疗有效地延迟了放疗后12周的纤维化发展。乌司他丁,甲基强的松龙或两者均可减轻PIAD的辐射诱发的增加(P <0.05或P <0.01)。与R组相比,在放疗后9周,用乌司他丁,甲基强的松龙或两者联合治疗可显着降低TNF-α的表达,但不降低TGF-β1的表达(P <0.01)。乌利他汀和/或甲基强的松龙可有效降低RILI后肺组织中的TNF-α水平,并抑制炎症反应和纤维化的发展。

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