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慢性阻塞性肺疾病急性加重痰热证与痰湿证动物模型炎症因子表达的比较研究 被引量:10

A comparative study of inflammatory factor expression of phlegm-heat syndrome and phlegm-dampness syndrome model with acute exacerbation of chronic obstructive pulmonary disease
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摘要 目的从炎症因子表达方面揭示慢性阻塞性肺疾病急性加重(AECOPD)痰热证与痰湿证动物模型的特点。方法按随机数字表法将48只Wistar大鼠分为正常对照组、AECOPD组、AECOPD痰热证组和AECOPD痰湿证组,每组12只。采用免疫组化法测定肺组织白细胞介素(IL-1β、IL-6、IL-10)、肿瘤坏死因子-α(TNF-α)的蛋白表达,采用逆转录-聚合酶链反应(RT-PCR)测定肺组织IL-1β、IL-10的mRNA表达。结果AECOPD组、AECOPD痰热证组和AECOPD痰湿证组炎症因子mRNA及蛋白表达均显著高于正常对照组。与AECOPD组比较,AECOPD痰热证组、AECOPD痰湿证组肺组织IL-1β、TNF-α、IL-6蛋白和IL-1βmRNA表达显著升高(IL-1β蛋白:6.26±2.43、8.20±2.61比4.30±2.38,TNF-α蛋白:10.28±2.64、10.67±2.68比7.47±2.90,IL-6蛋白:8.13±3.03、10.45±3.37比5.66±3.18,IL-1βmRNA:0.41±0.03、0.48±0.05比0.35±0.04,均P〈0.01),IL-10的蛋白和mRNA表达显著降低(IL-10蛋白:7.00±1.89、4.70±2.31比9.33±2.58,IL-10mRNA:0.43±0.05、0.35±0.03比0.52±0.06,P〈0.05或P〈0.01)。与AECOPD痰热证组比较,AECOPD痰湿证组的IL-1β蛋白和wRNA、IL-6蛋白表达明显增加,IL-10蛋白和mRNA表达明显减弱(均P〈0.05)。结论AECOPD痰湿证较AECOPD痰热证IL-1β、IL-6表达增强,IL-10表达减弱,这可能是痰湿证肺组织损伤严重且临床恢复缓慢的主要原因,有待于进-步研究。 Objective To reveal characteristic of phlegm-heat syndrome and phlegm-dampness syndrome of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) from expression of inflammatory factor. Methods Forty-eight Wistar rats were randomly divided into four groups (each n = 12): normal control group, AECOPD group, phlegm-heat syndrome of AECOPD group (PHs group) and phlegm-dampness syndrome of AECOPD group (PDs group). The expressions of interleukins (IL-1β, IL-6, IL-10), tumor necrosis factor-α(TNF-α) proteins in lung tissue were detected by immunohistochemical staining method. IL-1β mRNA and IL-10 mRNA expressions were measured by reverse transcription- polymerase chain reaction (RT-PCR). Results The mRNA and protein expressions of inflammatory factors in lung tissue in AECOPD group, PHs group and PDs group were remarkably enhanced compared with those in normal control group. Compared with AECOPD group, the protein expressions of IL-1β, TNF-α and IL-6 and the mRNA expression of IL1-βin lung tissue in PHs group and PDs group were markedly enhanced (IL-1β protein: 6.26 ± 2.43, 8.20 ± 2.61 vs. 4.30 ± 2.38, TNF-α protein: 10.28 ± 2.64, 10.67 ± 2.68 vs. 7.47 ± 2.90,IL-6 protein: 8.13 ± 3.03, 10.45 ± 3.37 vs. 5.66 ± 3.18, IL-1β mRNA: 0.41 ± 0.03, 0.48 ± 0.05 vs. 0.35 ± 0.04, all P〈0.01 ), and the expressions of IL-10 protein and IL-10 mRNA were obviously weakened (IL-10 protein: 7.00 ± 1.89, 4.70 ± 2.31 vs. 9.33 ± 2.58, IL-10 mRNA: 0.43 ± 0.05, 0.35 ± 0.03 vs. 0.52 ± 0.06, P〈0.05 or P〈0.01 ). The protein expressions of IL-1β and IL-6 proteins and the mRNA expression of IL-1β in PDs group were significantly higher than those in PHs group, while the expressions of IL-10 protein and IL-10 mRNA were evidently lowered (all P〈0.05). Conclusions There were more strong expressions of IL-1β and IL-6 and more weaken expressions of IL-10 in phlegm-dampness syndrome than in phlegm-heat syndrome, which may be one of the main reason of serious damage in lung tissue and delayed recovery of the patient with phlegm-dampness syndrome of AECOPD. All the above findings need further investigation.
出处 《中华危重病急救医学》 CAS CSCD 北大核心 2013年第6期343-346,共4页 Chinese Critical Care Medicine
基金 国家自然科学基金项目(81202658,30772797)
关键词 肺疾病 阻塞性 慢性 急性加重期 痰湿证 痰热证 炎症因子 Chronic obstructive pulmonary disease Acute exacerbation Phlegm-dampness syndrome Phlegm-heat syndrome Inflammatory factor
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