CAJ | 학술논문

目的：探讨乌司他丁（UTI）对脂多糖（LPS）致大鼠急性肺损伤（ALI）组织糖皮质激素受体（GR）的影响，并了解其可能机制。方法清洁级成年雄性SD大鼠54只，随机分为3组：空白对照组（Con组，n＝18），LPS组（n＝18），脂多糖+乌司他丁组（LPS＋UTI组，n＝18）。各组又按照不同的时间点被分为4 h、8 h、12 h三个亚组。在各时间点处死大鼠，利用Western blot检测大鼠肺组织中GR的表达，实时荧光定量PCR检测GR mRNA的表达，同时酶联免疫吸附法（ELISA）检测肺组织匀浆液中肿瘤坏死因子（TNF）-α和白细胞介素（IL）-10的浓度以及肺组织病理学的变化。结果与对照组相比，LPS组GR蛋白表达在各时间点降低（P＜0.05），LPS＋UTI组GR蛋白在各时间点的表达水平高于LPS组，低于Con组（P＜0.05）；与对照组相比，LPS组GR mRNA表达降低（P＜0.05），LPS＋UTI组GR mRNA在各时间点的表达水平略高于LPS组（P＞0.05），低于Con组（P＜0.05）；与对照组相比，LPS组TNF-α的表达在各时间点升高（P＜0.05），LPS＋UTI组TNF-α的表达水平在各时间点低于LPS组，高于Con组（P＜0.05）；与对照组相比，LPS组IL-10的表达在各时间点升高（P＜0.05），LPS＋UTI 组 IL-10的表达水平在各时间点高于 LPS组（P＜0.05）。组织病理学检查显示：LPS 组肺组织见肺泡结构破坏，炎性细胞浸润，肺泡间隔增宽，出血，水肿，LPS＋UTI组肺组织病理损害较LPS组明显减轻。结论 UTI能提高GR的表达；TNF-α和IL-10出现高峰的时间不同。
목적：탐토오사타정（UTI）대지다당（LPS）치대서급성폐손상（ALI）조직당피질격소수체（GR）적영향，병료해기가능궤제。방법청길급성년웅성SD대서54지，수궤분위3조：공백대조조（Con조，n＝18），LPS조（n＝18），지다당+오사타정조（LPS＋UTI조，n＝18）。각조우안조불동적시간점피분위4 h、8 h、12 h삼개아조。재각시간점처사대서，이용Western blot검측대서폐조직중GR적표체，실시형광정량PCR검측GR mRNA적표체，동시매련면역흡부법（ELISA）검측폐조직균장액중종류배사인자（TNF）-α화백세포개소（IL）-10적농도이급폐조직병이학적변화。결과여대조조상비，LPS조GR단백표체재각시간점강저（P＜0.05），LPS＋UTI조GR단백재각시간점적표체수평고우LPS조，저우Con조（P＜0.05）；여대조조상비，LPS조GR mRNA표체강저（P＜0.05），LPS＋UTI조GR mRNA재각시간점적표체수평략고우LPS조（P＞0.05），저우Con조（P＜0.05）；여대조조상비，LPS조TNF-α적표체재각시간점승고（P＜0.05），LPS＋UTI조TNF-α적표체수평재각시간점저우LPS조，고우Con조（P＜0.05）；여대조조상비，LPS조IL-10적표체재각시간점승고（P＜0.05），LPS＋UTI 조 IL-10적표체수평재각시간점고우 LPS조（P＜0.05）。조직병이학검사현시：LPS 조폐조직견폐포결구파배，염성세포침윤，폐포간격증관，출혈，수종，LPS＋UTI조폐조직병리손해교LPS조명현감경。결론 UTI능제고GR적표체；TNF-α화IL-10출현고봉적시간불동。
ObjectiveTo investigate the effect of Ulinastatin on the expression of glucocorticoid receptor during the course of acute lung injury induced by Lipopolysaccharide endotoxin in rats and to explore the underlyling mechanisms.Methods 54 male Sprague-Dawley rats were randomly divided into three groups with 18 mice each group: control group (Con group), lipopolysaccharide group (LPS group), lipopolysaccharide plus ulinastatin group (UTI group). All groups were then divided into three subgroups of 4 h, 8 h, 12 h (n=6). Rats were killed at indicated time points, and the protein and mRNA expression of GR in the lung were detected by Western blot and Real Time fluorescent quantitative PCR. The levels of TNF-α and IL-10 were also tested by ELISA. The pathology of lung tissue was evaluated by HE staining. Results Compared with control group, the protein expression levels of GR in LPS group were significantly lower. The protein expression levels of GR in UTI group were higher than those in LPS group, but lower than those in control group at all indicated time points. Compared with control group, the expression levels of GR mRNA in LPS group were significantly lower at all indicated time points. The expression levels of GR mRNA in UTI group were slightly higher than those in LPS group. No significant differences were found between UTI and LPS group in the expression levels of GR mRNA at all time points. Compared with control group, the expression levels of TNF-α in LPS group were significantly higher at all time points. The expression levels of TNF-α in UTI group were lower than those in LPS group at all time point. Compared with control group, the expression levels of IL-10 in LPS group were higher at all time points. In UTI group, the expression levels of IL-10 were higher than those in LPS group at all time points. Lung hispathology: necrotic abscission cells increased in alveolar space, inflammatory cells infiltration and lung interstitial edema appeared in LPS group. However, pathological changes in UTI group were milder than those in LPS group.ConclusionUTI could promote the expression of GR. Levels of TNF-α and IL-10 peaked at different time points.