CAJ | 학술논문

目的：观察黄芪对急性肺损伤的保护作用并探讨肺组织中细胞间粘附分子-1（ICAM-1）、血管细胞间粘附分子-1（VCAM-1）的表达在急性肺损伤（ALI）中的作用。方法 Wistar 大鼠30只，随机分为正常对照组、模型组和黄芪组，每组10只。建立急性肺损伤模型，给药6 h 后处死所有大鼠，取出肺组织做病理学观察，并检测各组肺组织髓过氧化物酶（MPO）、超氧化物歧化酶(SOD)活性变化以及 ICAM-1、VCAM-1的表达变化。结果与正常对照组相比，模型组、黄芪组的 MPO 活性和 ICAM-1、VCAM-1表达均显著增强（P <0.05或 P <0.01），且黄芪组上述指标明显低于模型组（P <0.05或 P <0.01）；急性肺损伤后，肺组织中的 SOD 活性明显降低（P <0.05或 P <0.01），但经黄芪处理后的黄芪组 SOD 活性水平又明显的增强（P <0.05)。结论黄芪能对急性肺损伤能起到有效的保护作用，其机制可能与其调节 ICAM-1、VCAM-1表达和提高 SOD 活性有关。
목적：관찰황기대급성폐손상적보호작용병탐토폐조직중세포간점부분자-1（ICAM-1）、혈관세포간점부분자-1（VCAM-1）적표체재급성폐손상（ALI）중적작용。방법 Wistar 대서30지，수궤분위정상대조조、모형조화황기조，매조10지。건립급성폐손상모형，급약6 h 후처사소유대서，취출폐조직주병이학관찰，병검측각조폐조직수과양화물매（MPO）、초양화물기화매(SOD)활성변화이급 ICAM-1、VCAM-1적표체변화。결과여정상대조조상비，모형조、황기조적 MPO 활성화 ICAM-1、VCAM-1표체균현저증강（P <0.05혹 P <0.01），차황기조상술지표명현저우모형조（P <0.05혹 P <0.01）；급성폐손상후，폐조직중적 SOD 활성명현강저（P <0.05혹 P <0.01），단경황기처리후적황기조 SOD 활성수평우명현적증강（P <0.05)。결론황기능대급성폐손상능기도유효적보호작용，기궤제가능여기조절 ICAM-1、VCAM-1표체화제고 SOD 활성유관。
Objective To investigate the protective effects of Astragalus on acute lung injury and to explore the role of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on acute lung injury in rats. Methods 30 Wistar rats were randomly divided into control group, model group and Astragalus group (n=10 , respectively). All rats were sacrificed 6 h after administration of Astragalus, removed lung tissue for pathological observation, and examined the expression of myeloperoxidase (MPO), superoxide dismutase (SOD) activity and ICAM-1, VCAM-1 in each group. Results Compared with control group, MPO activity and ICAM-1, VCAM-1 expression were significantly increased in model group and Astragalus group (P <0.05 or P <0.01 respectively).However, in Astragalus group, MPO activity and ICAM-1, VCAM-1 expression were significantly lower than that of model group (P <0.05 or P <0.01 respectively). Lung tissue SOD activity was significantly lower after lung injury (P <0.05 or P <0.01 respectively), but it was significantly enhanced after treatment with Astragalus (P <0.05). Conclusion Astragalus can play a protective effect on ALI, and the mechanism may relate to regulate the expression of ICAM-1, VCAM-1 and increase the activity of SOD.