论文部分内容阅读
目的 探讨内源性一氧化碳 (CO)在哮喘中的变化及其调节机制。 方法 5 0只豚鼠随机分成 5组 ,建立哮喘豚鼠模型 ,其中 3组分别使用地米松、血红素氧合酶 1(HO- 1 )特异性激动剂血晶素和抑制剂锡原卟啉 ,余为哮喘组和正常对照组。用分光光度法检测血一氧化碳血红蛋白 (COHb)含量和肺组织HO- 1 活性 ,免疫组化染色观察肺组织HO- 1 蛋白表达等。 结果 哮喘组全血COHb为 4 94± 2 15 % ;肺HO- 1 活性为 881± 36 1pmol/(mg .protein·h) ,分别较正常组有显著性差异 (t=4 5 8～ 10 19,P <0 0 1) ,肺HO- 1 蛋白增加。血晶素激动组较哮喘组略高 (P >0 0 5 )。锡原卟啉抑制和地塞米松预防组较哮喘组明显降低 (t =4 43～ 8 83,P <0 0 1)。血COHb与肺组织HO- 1 活性水平呈正相关 (r =0 90 ,P <0 0 0 1)。 结论 哮喘时体内HO- 1 蛋白和活性增加 ,导致内源性CO水平升高
Objective To investigate the changes of endogenous carbon monoxide (CO) in asthma and its regulatory mechanism. Methods Fifty guinea pigs were randomly divided into five groups. Asthmatic guinea pig models were established. Three of the three groups were treated with gemcitabine, heme oxygenase 1 (HO-1) specific agonist hemin and tin protoporphyrin Asthma group and normal control group. The content of hemoglobin (COHb) and the activity of HO-1 in lung tissue were detected by spectrophotometry. The expression of HO-1 protein in lung tissue was observed by immunohistochemical staining. Results The whole blood COHb in asthma group was 4 94 ± 2 15%. The activity of lung HO-1 was 881 ± 36 1 pmol / (mg · protein · h), which were significantly different from the normal group (t = 458-1019 , P <0.01), lung HO-1 protein increased. Hemocyanin group was slightly higher than asthma group (P> 0.05). Protoporphyrin inhibition and dexamethasone prevention groups were significantly lower than the asthma group (t = 4 43 ~ 8 83, P 0 01). COHb levels in blood were positively correlated with HO-1 activity in lung tissue (r = 0 90, P 0 01). Conclusions The increase of HO-1 protein and activity in asthma results in the increase of endogenous CO level