CAJ | 학술논문

目的肺表面活性物质蛋白D(SP-D)被认为是急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)有价值的生物指标,但在急性肺损伤早期,肺组织SP-D的变化特征仍不清楚.该研究旨在探究脂多糖(LPS)诱导的SD幼鼠急性肺损伤时SP-D,SP-D mRNA的时序变化及肺泡Ⅱ型上皮细胞及板层小体的超微结构的变化.方法腹腔内注射LPS建立急性肺损伤模型.注射后6,12,24,36,48,72 h各处死8只大鼠.Western blot和RT-PCR方法测定肺组织SP-D和SP-D mRNA的含量.透射电子显微镜研究肺泡Ⅱ型上皮细胞超微结构的变化.结果LPS注射12 h后SP-D和SP-D mRNA含量均开始下降.SP-D mRNA于注射LPS后24～36 h降到最低.SP-D在48 h达最低点.透射电镜显示急性肺损伤组板层小体出现多样变形,特别是在注射后48 h.LPS导致板层小体的体积增大、数量减少,伴有大量空泡样变.结论在LPS诱导的急性肺损伤的早期SP-D的波动变化呈时间依赖性.肺组织SP-D在48 h时水平最低,此时伴有肺泡Ⅱ型上皮细胞严重的多形性变.在ALI发病初期,肺组织低水平的SP-D与较差的临床预后有关.
목적폐표면활성물질단백D(SP-D)피인위시급성폐손상(ALI)화급성호흡군박종합정(ARDS)유개치적생물지표,단재급성폐손상조기,폐조직SP-D적변화특정잉불청초.해연구지재탐구지다당(LPS)유도적SD유서급성폐손상시SP-D,SP-D mRNA적시서변화급폐포Ⅱ형상피세포급판층소체적초미결구적변화.방법복강내주사LPS건립급성폐손상모형.주사후6,12,24,36,48,72 h각처사8지대서.Western blot화RT-PCR방법측정폐조직SP-D화SP-D mRNA적함량.투사전자현미경연구폐포Ⅱ형상피세포초미결구적변화.결과LPS주사12 h후SP-D화SP-D mRNA함량균개시하강.SP-D mRNA우주사LPS후24～36 h강도최저.SP-D재48 h체최저점.투사전경현시급성폐손상조판층소체출현다양변형,특별시재주사후48 h.LPS도치판층소체적체적증대、수량감소,반유대량공포양변.결론재LPS유도적급성폐손상적조기SP-D적파동변화정시간의뢰성.폐조직SP-D재48 h시수평최저,차시반유폐포Ⅱ형상피세포엄중적다형성변.재ALI발병초기,폐조직저수평적SP-D여교차적림상예후유관.
Objective Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), but the alterations of SP-D in lung tissues in the early course of ALI remain unknown. This study was designed to explore the temporal fluctuations of SP-D and SP-D mRNA in young rats with ALI induced by lipopolysaccharide (LPS) , as well as the alterations of ultrastructures of alveolar type Ⅱ (ATⅡ) cells. Methods Rat ALI models were established by intraperitoneal injection of LPS (4 mg/kg). The rats were sacrificed at 6, 12, 24, 36, 48 and 72 hrs after LPS injection (8 rats each time point). Western blot and RT-PCR were employed to detect the contents of SP-D and SP-D mRNA in lung tissues. The ultrastructures of AT Ⅱ cells were studied with transmission electron microscopy. Results Both SP-D mRNA and SP-D levels decreased after 12 hrs of LPS administration. The SP-DmRNA level reached a nadir at 24-36 hrs, but the SP-D level was reduced to its nadir by 48 hrs after LPS administration. LPS resulted in the alterations of lamellar bodies (LBs) in size ( multilamellar forms), density (vacuole-like deformity) and number. The alterations of ultrastructures of AT Ⅱ cells were most significant at 48 hrs. The clinical symptoms of ALI rats were most severe at 48 hrs. Conclusions The alterations of the SP-D level were timedependent in the early course of LPS-induced ALI. The lowest level of SP-D occurred at 48 hrs while severe multideformities of AT Ⅱ cells were presented. A decreased level of SP-D in the lungs in the early stage of ALI may be associated with a worse clinical outcome.