龙麻金宁方对热哮大鼠肺组织PKBmRNA、α-SMAmRNA表达的影响

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目的:研究龙麻金宁方对热哮大鼠气道重塑及其肺组织中蛋白激酶B(PKBm RNA)、成纤维细胞α-平滑肌肌动蛋白(α-SMA m RNA)、血小板衍生因子(PDGF)、I、III胶原蛋白表达水平的影响。方法:雄性SD大鼠,70只,随机分成以下7组:正常组、模型组、地塞米松组、麻杏石甘汤组以及龙麻金宁高、中、低剂量组,每组10只。在第1天和第8天,以10%卵蛋白腹腔注射致敏及细菌脂多糖(LPS)滴鼻制热(终浓度400μg·m L-1)复制大鼠热哮模型。第15天开始1%卵蛋白雾化激发,连续7 d,第21天模型复制成功,开始治疗。正常组、模型组每天给予等量蒸馏水灌服,地塞米松组、麻杏石甘汤组、龙麻金宁高、中、低剂量组按人体与大鼠体表面积换算比折算剂量灌胃,灌胃4周后解剖大鼠并取出肺组织。采用HE染色法观察肺组织的病理形态学改变;采用免疫组化法观察肺组织的中、小气道I、III胶原蛋白的阳性表达;采用酶联免疫吸附反应定量肺组织的PDGF含量;采用逆转录-聚合酶链反应以半定量测定PKBm RNA、α-SMA m RNA的表达丰度。结果:与正常组比较,模型组发生明显肺组织炎症反应和气道重塑现象,α-SMAm RNA、PKBm RNA、PDGF、I、III胶原表达水平显著升高(P<0.01);龙麻金宁高、中、低剂量治疗组与模型组比较,α-SMAm RNA、PKBm RNA、PDGF、I、III胶原表达水平显著降低(P<0.01)。结论:龙麻金宁明显减轻热哮大鼠气道炎症反应,抑制热哮大鼠肺组织中α-SMA m RNA、PKBm RNA、PDGF、I、III胶原的表达,延缓气道重塑而治疗哮喘。 Objective: To investigate the effects of Longmai Jinning Fang on airway remodeling and expression of PKBm RNA, α-SMA m RNA and platelet-derived factor (PDGF), I, III collagen expression levels. Methods: Seventy male Sprague-Dawley rats were randomly divided into the following 7 groups: normal group, model group, dexamethasone group, Maxing Shigan Decoction group, and Longmainingjinning high, medium and low dose groups . On day 1 and day 8, the rat model of asthma was reproduced by intraperitoneal injection of 10% ovalbumin and bacterial lipopolysaccharide (LPS) intranasally (final concentration 400 μg · m L -1). On the 15th day, 1% ovalbumin was initiated and challenged for 7 days. On the 21st day, the model was successfully replicated and the treatment was started. Normal group and model group were given equal volume of distilled water daily, dexamethasone group, Maxing Shigan Decoction group, Longma Jinning high, medium and low dose groups according to the body and the rat body surface area conversion ratio conversion dose gavage, Four weeks after gavage, the rats were dissected and lung tissue was removed. The pathological changes of lung tissue were observed by HE staining. The positive expression of I and III collagen in lung tissue was observed by immunohistochemical method. The level of PDGF in lung tissue was quantified by enzyme-linked immunosorbent assay Polymerase chain reaction to semi-quantitative determination of PKBm RNA, α-SMA m RNA expression abundance. Results: Compared with the normal group, the lung tissue inflammatory reaction and airway remodeling were obvious in the model group. The expression of α-SMAm RNA, PKBm RNA, PDGF, I, III collagen was significantly increased (P <0.01) Compared with the model group, the expression of α-SMAm RNA, PKBm RNA, PDGF, I and III collagen in high, middle and low dose treatment groups was significantly decreased (P <0.01). Conclusion: Long Ma Jin Ning significantly reduces the airway inflammation in the heat-induced asthmatic rats, and inhibits the expression of α-SMA m RNA, PKBm RNA, PDGF, I and III collagen in the lungs of rats with hyperthermia and delays the airway remodeling asthma.
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