【摘要】 目的探讨654-2联合甲基强的松龙对急性呼吸窘迫综合征(ARDS)大鼠肺泡Ⅱ型上皮细胞的影响。方法通过建立油酸诱导的大鼠ARDS模型,分别使用654-2、甲基强的松龙药物干预,测定各组各时段肺组织干湿比和血清中TNF-α、IL-1的水平,并观察光镜下肺组织病理学及电镜下肺泡Ⅱ型上皮细胞的改变。结果甲基强的松龙组大鼠肺组织干湿比及血清中TNF-α、IL-1水平改变与模型未干预组比较,差异有极显著性(P<0.01),在24 h组时其与654-2组比较,明显改善,差异具有显著性(P<0.05);光镜结果显示:甲基强的松龙对肺组织的保护作用优于654-2;24 h光镜下肺组织病理评分甲基强的松龙组(8.92±3.62)分与654-2组(13.29±2.98)分比较,差异具有显著性(P<0.05);电镜下甲基强的松龙干预组较654-2干预组肺Ⅱ型细胞包膜完整,板层小体空泡现象较少,细胞核较完整,染色质较均匀。说明甲基强的松龙保护肺Ⅱ型细胞的作用强于654-2。结论甲基强的松龙可通过抑制细胞因子的失控性释放,以减轻大鼠肺Ⅱ型细胞的功能损伤,较654-2显示出更好的肺保护作用。更多还原

【Abstract】 Objective To investigate the impact of the alveolar type Ⅱ cells for Anisodamine(654-2) associated with Methylprednisolone(MP) on oleic acid-induced acute respiratory disdress syndrome(ARDS) in rats.Methods The ARDS model in rats with oleic acid-induced was treated the by the 654-2 and MP respectively.alveolar type II cells were measured at different fixed time points in different groups,such as TNF-α,IL-1 in serum.At the same time,the pathologic structure of lung was observed under the optical microscope,and the changes of the alveolar type Ⅱ cells were observed under Electron microscopy.Results There were statistically significant differences for the TNF-α,IL-1 in serum and lung tissue dry to wet scores in MP intervented group compared with the non-intervented group of model group(P<0.01).Compared with those 654-2 group,there were statistically significant differences in 24h(P<0.05).There were also statistically significant differences between the 654-2 group and MP groups(P<0.05).The results showed that the protective effects of MP to lung tissues superior to that of 654-2.The lung tissue pathology score have change clearly in 24h group which the value were 8.92±3.62 and 13.29±2.98 respectively.The change of alveolar type II cells envelope,lamellar body vacuolization phenomenon,nucleus,and chromatin also better than 654-2 group.Conclusion The MP and 654-2 can protect the lung in the oleic acid-induced ARDS model in rats.But the effect of MP is better than that of 654-2.The protective mechanisms maybe through inhabit the overflowing of inflammation factors and mitigate the alveolar type Ⅱ cells injury in lung.更多还原