不同功率微波照射对博莱霉素诱导的肺纤维化大鼠的效应研究

关键词：微波  肺纤维化  炎症

Keywords:microwave  pulmonary fibrosis  inflammation

摘要：

      摘要 目的：研究不同功率微波照射（electromagnetic wave irradiation）对博莱霉素（bleomycin， BLM）诱导大鼠肺纤维化（pulmonary fibrosis）不同病程阶段的效应。 方法：气管注入5mg/kg博莱霉素构建肺纤维化模型。将大鼠随机分为4组，正常对照组、模型组、10min小功率照射组、20min大功率照射组；在造模7d、14d、28d，两组微波照射组分别接受不同功率的微波照射，正常对照组和模型组不接受微波照射。HE、Masson、天狼猩红染色及组织免疫组化染色法观察肺组织病理学改变以及纤维化相关分子（α-SMA、COL1a1）的表达，qRT-PCR检测大鼠肺组织中的炎症因子水平，PET-CT检测大鼠的肺组织的代谢情况。 结果：①组织病理染色以及免疫组化结果显示，随着病程的进展，模型组肺组织以先增强后稳定的肺泡炎和不断增强的纤维化病变为主。在造模28d，小功率微波照射可明显改善肺泡炎和肺纤维化（肺泡炎评分P=0.0078、肺纤维化评分P=0.0248、α-SMA P＜0.0001、COL1a1 P=0.0449），大功率微波照射组仅α-SMA表达下调（P＜0.0001）。不同功率的微波照射对肺纤维化改变未显示出显著性差异。②qRT-PCR结果显示，在造模28d，模型组的大鼠肺组织中炎症因子mRNA表达均增高（P＜0.05），微波照射可降低肺纤维化大鼠肺组织炎症因子的表达水平（小功率组 IL-1β P=0.0022、IL-6 P=0.0221、TNF-α P=0.0199，大功率组 IL-1β P=0.0276、IL-13 P=0.0276）。不同功率的微波照射未显示出显著性差异。③PET-CT结果显示，与正常对照组相比，造模28d，模型组大鼠肺组织代谢活动增强（P=0.0485），微波照射可以增强肺纤维化大鼠的肺组织代谢能力（大功率组P=0.0357）。不同功率的微波照射对大鼠的肺组织代谢能力未显示出显著性差异。 结论：微波照射（小功率90V/m、大功率250V/m）可能通过调控造模28d的肺纤维化大鼠炎症因子和纤维化相关因子的表达发挥抗炎抗纤维化作用。

Abstract:

      Abstract Objective：To explore the effect of different power microwave irradiation on bleomycin （BLM）-induced pulmonary fibrosis in rats. Method：The rat model of pulmonary fibrosis was established by tracheal injection of 5 mg/kg bleomycin. The rats were randomly divided into 4 groups： the normal control group， the model group， the 10min low power irradiation group， the 20min high power irradiation group. At 7d， 14d and 28d after modeling， two microwave irradiation groups received microwave irradiation with different power， while the normal control group and the model group did not receive any irradiation. The pathological changes and the expression levels of fibrosis-related molecules（α-SMA， COL1a1） were detected by HE， Masson and IHC of lung tissues. The mRNA expression levels of inflammation-related molecules in lung tissues of rats were detected by qT-PCR. The metabolism of lung tissues was detected by F18-FDG PET-CT. Result：①The results of histopathological staining and immunohistochemistry showed that with the progress of the disease， the lung tissues of model group mainly exhibited enhanced and then stable alveolitis and enhanced fibrotic lesions. At 28 days after model establishment， low power microwave irradiation could significantly improve alveolitis and pulmonary fibrosis （alveolitis score P=0.0078， pulmonary fibrosis score P=0.0248， α-SMA P<0.0001， COL1a1 P=0.0449）， and the expression of α-SMA was down-regulated in high power microwave irradiation group （P<0.0001）. Microwave irradiation with different power showed no different effect on the pulmonary metabolism. ②qRT-PCR results showed that the mRNA expressions of inflammatory factors in the lung tissues of the model group were increased at 28 days after modeling （P<0.05）. Microwave irradiation could reduce the expression levels of inflammatory factors in lung tissue of rats with pulmonary fibrosis （the low-power group IL-1β P=0.0022， IL-6 P=0.0221， TNF-α P=0.0199， the high-power group IL-1β P=0.0276， IL-13 P=0.0276）. Microwave irradiation with different power showed no statistical difference. ③PET-CT results showed that compared with the normal control group， the metabolic activity of lung tissue in the model group was enhanced 28 days after modeling （P=0.0485）. Microwave irradiation could enhance the metabolic capacity of lung tissue in a power-dependent manner （the high-power group P=0.0357）. Microwave irradiation with different power has no different effect on the metabolic ability of lung tissue. Conclusion：Microwave irradiation （low-power 90V/m， high-power 250V/m） may exert anti-inflammatory and anti-fibrosis effects by regulating the expression of inflammatory factors and fibrosis-related factors at 28d after modeling.