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MiR-143-5p调节MAPK/ERK途径对大鼠肺纤维化模型肺组织中炎症反应的影响 被引量:2

Effect of MiR-143-5p regulating MAPK/ERK pathway on inflammation in lung tissue of pulmonary fibrosis rat model
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摘要 目的 探索MiR-143-5p通过MAPK/ERK途径改善肺纤维化大鼠模型气道炎症反应的效果及机制。方法 6~8周龄雌性Sprague-Dawley大鼠45只随机分为对照组、造模组、miR-143-5P组每组15只。造模组和miR-143-5P组给予博来霉素5 mg/kg气管注射,对照组给予等量的生理盐水气管注射;造模后第8天miR-143-5P组给予agomiR-143-5P,对照组和造模组给予agomiR-NC。观察大鼠一般情况、存活率。检测大鼠呼吸频率(F)、潮气量(TV)、呼气峰流量(PEF)、吸气峰流量(PIF)和呼气时间(TE),ELISA法检测支气管肺泡灌洗液中炎症因子TNF-α和IL-1β的水平,对肺组织进行HE染色,Western blot检测大鼠肺组织中p-ERK和ERK的蛋白表达。结果 miR-143-5P组大鼠一般情况改善,生存率有所提高。肺功能检测提示F、TV、PEF、PIF和TE均较造模组改善(P<0.05),而吸气时间(TI)与造模组相比差异无统计学意义(P>0.05);HE染色提示miR-143-5P组肺组织病理变化较造模组改善;造模组和miR-143-5P组大鼠支气管肺泡灌洗液中炎症因子TNF-α和IL-1β的水平高于对照组(P<0.05),而miR-143-5P组均低于造模组(P<0.05);Western blot法检测p-ERK和ERK蛋白表达水平并计算p-ERK/ERK比率发现,造模组和miR-143-5P组p-ERK/ERK比率高于对照组(P<0.05),而miR-143-5P组低于造模组(P<0.05)。结论 miR-143-5P可能通过抑制MAPK/ERK信号通路改善PF大鼠模型的肺功能,减轻气道的炎症反应。 ObjectiveTo explore the effect and mechanism of miR-143-5p on airway inflammation in rat model of pulmonary fibrosis by MAPK/ERK pathway.MethodsForty-five female Sprague-Dawley(SD)rats aged 6-8 weeks were randomly divided into control group,model group and miR-143-5p group with 15 rats in each group. The model group and miR-143-5p group were given bleomycin 5 mg/kg tracheal injection,while the control group was given the same amount of normal saline. On the 8th day after modeling,the miR-143-5p group was given Agomir-143-5p,and the control group and the modeling group were given Agomir-NC,once every 3 days through caudal vein,for a total of 21 days. The general condition and survival rate of rats were observed. Lung function of rats was detected. The levels of inflammatory cytokine TNF-αand IL-1β in bronchoalveolar lavage fluid were detected by ELISA. The protein expressions of p-ERK and ERK in lung tissues of rats were detected by Western blot.ResultsThe general condition and survival rate of miR-143-5p group were improved. Lung function test showed that respiratory frequency(F),tidal volume(TV),peak expiratory flow(PEF),peak inspiratory flow(PIF)and expiratory time(TE)were all improved compared with the model group(P<0.05),while inspiratory time(TI)had no significant difference compared with the model group(P>0.05). He staining indicated that the pathological changes of lung tissue in miR-143-5p group were improved compared with those in the model group. The levels of inflammatory cytokine TNF-α and IL-1β in bronchoalveolar lavage fluid of rats in model group and miR-143-5p group were higher than those in control group(P<0.05),while those in miR-143-5p group were lower than those in model group(P< 0.05).Western blot method was used to detect p-ERK and ERK protein expression levels and calculate p-ERK/ERK ratio. It was found that the p-ERK/ERK ratio in the model group and miR-143-5p group was higher than that in the control group(P< 0.05),while that in the miR-143-5p group was lower than that in the model group(P<0.05).ConclusionmiR-143-5p may improve the lung function of PF rats by inhibiting the MAPK/ERK signaling pathway and reduce the airway inflammatory response.
作者 王平 王攀 WANG Ping;WANG Pan(The Second Department of Geriatrics,Hengshui People's Hospital,Hengshui,Hebei Prouince 053000,China)
出处 《解剖学研究》 CAS 2022年第3期208-212,共5页 Anatomy Research
关键词 肺纤维化 miR-143-5P 丝裂原活化蛋白激酶 细胞外调节蛋白激酶 Pulmonary fibrosis miR-143-5P Mitogen-activated protein kinases(MAPKs) Extracellular signal regulated kinase
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