南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2010年
1期
43-46
,共4页
余林中%刘建新%胡孔友%刁建新%王丽
餘林中%劉建新%鬍孔友%刁建新%王麗
여림중%류건신%호공우%조건신%왕려
凉膈散%急性肺损伤%内毒素%信号转导与转录激活子1
涼膈散%急性肺損傷%內毒素%信號轉導與轉錄激活子1
량격산%급성폐손상%내독소%신호전도여전록격활자1
Lianggesan%acute lung injury%endotoxin%signal transducer and activator of transeription 1
目的 观察凉膈散对内毒素致急性肺损伤(AL1)大鼠肺组织中的信号转导与转录激活子1(STAT1)的影响及其作用机制.方法 静脉注射内毒素脂多糖(LPS)制作大鼠急性肺损伤模型.将实验动物随机分为空白组、LPS组、LPS+凉膈散高、中、低剂量组、LPS+地塞米松组,LPS组义分为致伤后1、2、4、8、16h不同时间点组,用蛋白免疫印迹法测定大鼠肺组织STAT1及磷酸化STAT1的表达.结果 与空白组比较,LPS组STAT1蛋白在4 h、P-STAT1蛋白在2 h表达最显著(P<0.01),凉膈散各组及地塞米松组在2、4、8 h能显著下调STAT1及P-STAT1蛋白的表达,与LPS组比较,有统计学意义(P<0.05,P<0.01).结论 内毒素致急性肺损伤中存在STAT1异常表达,凉膈散各组通过下调STAT1及P-STAT1的表达,从而减轻LPS所致的急性肺损伤,这可能是凉膈散治疗急性肺损伤的机制之一.
目的 觀察涼膈散對內毒素緻急性肺損傷(AL1)大鼠肺組織中的信號轉導與轉錄激活子1(STAT1)的影響及其作用機製.方法 靜脈註射內毒素脂多糖(LPS)製作大鼠急性肺損傷模型.將實驗動物隨機分為空白組、LPS組、LPS+涼膈散高、中、低劑量組、LPS+地塞米鬆組,LPS組義分為緻傷後1、2、4、8、16h不同時間點組,用蛋白免疫印跡法測定大鼠肺組織STAT1及燐痠化STAT1的錶達.結果 與空白組比較,LPS組STAT1蛋白在4 h、P-STAT1蛋白在2 h錶達最顯著(P<0.01),涼膈散各組及地塞米鬆組在2、4、8 h能顯著下調STAT1及P-STAT1蛋白的錶達,與LPS組比較,有統計學意義(P<0.05,P<0.01).結論 內毒素緻急性肺損傷中存在STAT1異常錶達,涼膈散各組通過下調STAT1及P-STAT1的錶達,從而減輕LPS所緻的急性肺損傷,這可能是涼膈散治療急性肺損傷的機製之一.
목적 관찰량격산대내독소치급성폐손상(AL1)대서폐조직중적신호전도여전록격활자1(STAT1)적영향급기작용궤제.방법 정맥주사내독소지다당(LPS)제작대서급성폐손상모형.장실험동물수궤분위공백조、LPS조、LPS+량격산고、중、저제량조、LPS+지새미송조,LPS조의분위치상후1、2、4、8、16h불동시간점조,용단백면역인적법측정대서폐조직STAT1급린산화STAT1적표체.결과 여공백조비교,LPS조STAT1단백재4 h、P-STAT1단백재2 h표체최현저(P<0.01),량격산각조급지새미송조재2、4、8 h능현저하조STAT1급P-STAT1단백적표체,여LPS조비교,유통계학의의(P<0.05,P<0.01).결론 내독소치급성폐손상중존재STAT1이상표체,량격산각조통과하조STAT1급P-STAT1적표체,종이감경LPS소치적급성폐손상,저가능시량격산치료급성폐손상적궤제지일.
Objective To investigate the effect of Lianggesan on the expression of signal transducer and activator of transcription 1 (STAT1) in rats with lipopolysaccharide (LPS)-induced acute lung injury and explore the possible mechanisms of the therapeutic effects. Methods Endotoxemia was induced in Wistar rats by intravenous injection of LPS (5 mg/kg). The rats were randomly divided into 6 groups, namely the control group, acute lung injury group (LPS group), 3 Lianggesan groups treated at different doses, and LPS+DEX treatment group. Each group, except for the control group, was further divided into 5 subgroups and examined at 1, 2, 4, 8 and 16 h after LPS injection. Western blotting was used to detect the protein expression of STAT1 and p-STAT1 in the lung tissue. Results In LPS group, the expression of STAT1 began to increase at 1 h following LPS injection, reaching the peak level at 4 h; the peak expression ofp-STAT1 occurred at 2 h after LPS administration (P<0.01). Compared with LPS group, the 3 Lianggesan groups and DEX group showed significantly decreased expressions of STAT1 and p-STAT1 at 2, 4 and 8 h after LPS injection (P<0.05 or 0.01). Conclusion Abnormal expression of STAT1 occurs in the lung tissue in the event of ALI. Lianggesan can relieve LPS-induced acute lung injury in rats by decreasing the expression of STAT1 and p-STAT1.