| 引用本文:李莉，危蕾，王众福，张秀莲，钱叶长.蜂毒素抑制博莱霉素诱导小鼠肺纤维化的机制研究[J].世界中医药,2019,(03):. |
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| 蜂毒素抑制博莱霉素诱导小鼠肺纤维化的机制研究 |
| Study on the Mechanism of Melittin Inhibiting Pulmonary Fibrosis Induced by Bleomycin in Rats |
| 投稿时间：2018-12-26 |
| DOI：10.3969/j.issn.1673-7202.2019.03.018 |
| 中文关键词: 蜂毒素 抑制 博莱霉素 小鼠 肺纤维化 机制 TGF-β1/Smads通路 羟脯氨酸 |
| English Keywords:Melittin Inhibition Bleomycin Pulmonary fibrosis Mechanism TGF-β1/Smads pathway Hydroxyproline |
| 基金项目:2016年上海市卫生和计划生育委员会基金项目（20164Y0241）——CXCL14通过TGF-β/Smads通路影响肺纤维化的机制研究 |
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| 中文摘要: |
| 目的：观察蜂毒素对博莱霉素诱导小鼠肺纤维化的干预作用。方法：70只SPF级C57BL/6小鼠被随机分为正常组10只和模型组、地塞米松组、蜂毒素低剂量组、蜂毒素中剂量组、蜂毒素高剂量组各12只。除正常组外，均采用气管穿刺注入博莱霉素（BLM）制备肺纤维化小鼠模型。从术后第1天开始,地塞米松组按3 mg/kg的剂量腹腔注射，蜂毒素低、中、高剂量组分别给予5 μg/（kg·d）、10 μg/（kg·d）、20 μg/（kg·d），对照组和模型组给予等体积生理盐水灌胃，连续2周。分别于第7、第14天处死动物，收集小鼠外周血样本，通过ELISA方法检测血清转化生长因子(TGF-β1)、胶原蛋白I(CollagenI)、胶原蛋白III(CollagenIII)、基质金属蛋白酶2（MMP2）和基质金属蛋白酶9（MMP9）的水平。取肺组织进行苏木精-伊红（HE）分析，Masson染色和羟脯氨酸（HYP）评估以观察组织病理学变化和胶原沉积。采用实时荧光定量(Real-ime PCR)法和蛋白兔疫印迹法(Western blot)观察各组大鼠肺组织TGF-β1、Smad2、Smad3等蛋白和基因的表达变化。结果:与对照组比较，模型组大鼠肺纤维化明显，HYP、TGF-β1、CollagenI、CollagenI的含量升高(P<0.05)，肺组织TGF-β1、Smad2、Smad3蛋白和基因表达升高(P<0.05)；与模型组比较，蜂毒素中高剂量组血清HYP、TGF-β1、CollagenI、CollagenI的含量下降(P<0.05)，肺组织TGF-β1、Smad2、Smad3蛋白和基因表达降低，差异有统计学意义(P<0.05)。结论：蜂毒素可以减轻博来霉素诱导的小鼠肺纤维化的程度，其机制可能与抑制TGF-β1/Smads通路有关。 |
| English Summary: |
| To observe the effects of melittin on inhibiting pulmonary fibrosis induced by bleomycin in rats. Methods:Seventy SPF grade C57BL/6 rats were randomly divided into the normal group(n=10)and the model group，dexamethasone group and melittin low dose group，melittin middle dose group and melittin high dose group(n=12). In addition to the normal group，a rat model of pulmonary fibrosis was prepared by injecting bleomycin(BLM)into the trachea. From the first day after surgery，the dexamethasone group was intraperitoneally injected at a dose of 3 mg/kg，while the low，medium and high doses of melittin were administered to 5，10，and 20 μg/(kg·d） respectively. The control group and the model group were given an equal volume of saline for 2 weeks. The animals were sacrificed on the 7th and 14th day，respectively，peripheral blood samples of which were collected. ELISA was used to detect serum transforming growth factor(TGF-β1)，collagen I(Collagen I)，collagen III(Collagen III)，and matrix metalloproteinase 2(MMP2)and the level of matrix metalloproteinase 9(MMP9). Lung tissue was taken for hematoxylin-eosin(HE)analysis，Masson staining and hydroxyproline(HYP)evaluation to observe histopathological changes and collagen deposition. The expressions of TGF-β1，Smad2，Smad3 and other proteins and genes in lung tissue of each group were observed by Real-time PCR and Western blot. Results:Compared with the control group，the pulmonary fibrosis was significantly increased in the model group. The contents of HYP，TGF-β1，Collagen I and Collagen I were increased(P<0.05)，and the expression of TGF-β1，Smad2，Smad3 protein and gene in lung tissue was increased(P<0.05); Compared with the model group，the levels of serum HYP，TGF-β1，Collagen I，CollagenI in the high dose group of melittin decreased(P<0.05)，and TGF-β1，Smad2，Smad3 protein in lung tissue and gene expression was decreased(P<0.05). There was no statistically significant difference in the low-dose group. Conclusion:Melittin can effectively reduce the degeneration of pulmonary fibrosis induced by bleomycin，and its mechanism may be related to the regulation of TGF-β1/Smads pathway. |
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