| 郭浩淳,陈佳佳,濮娟,丁洲,郁汉旭,董磊,张海军,王万鹏.消旋山莨菪碱减轻小鼠放射性肺损伤的作用及分子机制研究[J].中华放射医学与防护杂志,2023,43(6):418-424 |
| 消旋山莨菪碱减轻小鼠放射性肺损伤的作用及分子机制研究 |
| Mechanism of racanisodamine on alleviating radiation-induced lung injury in mice |
| 投稿时间：2023-02-10 |
| DOI：10.3760/cma.j.cn112271-20230210-00032 |
| 中文关键词: 消旋山莨菪碱 放射性肺损伤 细胞衰老 炎症 纤维化 |
| 英文关键词:Racanisodamine Irradiation induced lung injury Cell senescence Inflammation Fibrosis |
| 基金项目:江苏省卫生健康委指导性课题（Z2020022）；淮安市自然科学研究计划项目（HAB202251） |
| 作者 | 单位 | E-mail | | 郭浩淳 | 东南大学医学院附属中大医院肿瘤科, 南京 210009 | | | 陈佳佳 | 南京医科大学康达学院附属涟水人民医院放疗科, 淮安 223400
扬州大学医学院临床学院 江苏省中西医结合老年病防治重点实验室, 扬州 225009 | | | 濮娟 | 南京医科大学康达学院附属涟水人民医院放疗科, 淮安 223400
扬州大学医学院临床学院 江苏省中西医结合老年病防治重点实验室, 扬州 225009 | | | 丁洲 | 南京医科大学康达学院附属涟水人民医院放疗科, 淮安 223400 | | | 郁汉旭 | 南京医科大学康达学院附属涟水人民医院放疗科, 淮安 223400 | | | 董磊 | 东南大学医学院附属中大医院肿瘤科, 南京 210009 | | | 张海军 | 东南大学医学院附属中大医院肿瘤科, 南京 210009 | | | 王万鹏 | 南京医科大学康达学院附属涟水人民医院放疗科, 淮安 223400
扬州大学医学院临床学院 江苏省中西医结合老年病防治重点实验室, 扬州 225009 | wangwanpeng123@163.com |
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| 中文摘要: |
| 目的 探讨消旋山莨菪碱对X射线致放射性肺损伤的保护作用及机制。方法 将20只C57BL/6小鼠按随机数表法分为对照组、模型组（照射）、给药组（消旋山莨菪碱）、治疗组（照射+消旋山莨菪碱），每组5只。给药组、治疗组照射前3天给予消旋山莨菪碱注射液腹腔注射（5 mg/kg），模型组、治疗组给予6 MV X射线，18 Gy单次全胸腔照射，构建放射性肺损伤小鼠模型，辐照后治疗组采取每隔1天给药，连续给药6周后处死小鼠并取材。HE染色检测肺组织病理形态；酶联免疫吸附法（ELISA）检测肺泡灌洗液和血清中肿瘤坏死因子α（TNF-α）、白介素6（IL-6）、白介素1β（IL-1β）细胞因子表达；细胞衰老β-半乳糖苷酶（SA-β-Gal）染色检测肺组织细胞衰老情况；Western blot检测核因子E2相关因子2（Nrf2）、磷酸化NRF2（p-Nrf2）、p62蛋白表达。结果 与模型组相比，治疗组肺组织HE病理评分减低（t=8.66，P<0.01）；肺泡灌洗液中炎性细胞数量减少（t=10.70，P<0.01）、蛋白浓度降低（t=6.75，P<0.01），血清TNF-α、IL-1β、IL-6表达减少（t=8.17、4.58、6.54，P<0.01）；肺组织SA-β-gal活性降低，且肺组织Nrf2、磷酸化Nrf2表达增强（t=6.42、7.30，P<0.01），而p62表达减少（t=4.62，P<0.01）。结论 消旋山莨菪碱可通过减轻炎症等途径发挥对X射线致放射性肺损伤的保护作用，其保护机制可能与激活Nrf2通路，逆转辐照所致的细胞衰老有关。 |
| 英文摘要: |
| Objective To investigate the protective effect of racanisodamine on lung injury in mice exposed to irradiation.Methods C57BL/6 mice were randomly divided into control group, racanisodamine group, 18 Gy irradiation group (model group) and racanisodamine combined with 18 Gy irradiation group (treatment group), with 5 mice in each group. The mice in the treatment group received racanisodamine (5 mg/kg) intraperitoneally 3 d before irradiation and contained the whole experiments. Then, single chest irradiation of 18 Gy X-rays was performed both in the model and treatment groups. The racanisodamine group and treatment group received racanisodamine intraperitoneally once a day until 6 weeks after irradiation. The mice were killed at 6 weeks after irradiation. The lung histopathology was observed by HE staining. Serum and bronchial alveolar lavage fluid (BALF) inflammatory cytokines such as TNF-α, IL-1β and IL-6 were determined by ELISA method. Cell senescence was detected by SA-β-Gal staining. The expressions of Nrf2, p-Nrf2 and p62 in lung tissue were performed by immunehistochemistry and Western blot assays.Results Compared with the model group, the scores of HE staining were decreased (t=8.66, P<0.01), the number of infiltrated inflammatory cells in BALF were decreased (t=10.70, P<0.01), and protein concentration in BALF had lower levels (t=6.75, P<0.01), the serum TNF-α, IL-1β and IL-6 were decreased significantly (t=8.17, 4.58, 6.54, P<0.01), the activity of SA-β-gal was decreased, and the expressions of Nrf2, p-Nrf2 were enhanced (t=6.42, 7.30, P<0.01), while the expression of p62 was reduced (t=4.62, P<0.01) in the treatment group.Conclusions Racanisodamine plays the protective effect of radiation-induced lung injury by alleviating inflammation associating with the activating of Nrf2-related pathway, which reversed radiation-induced cell senescence. |
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