摘要
目的 :探讨丹参对创伤性急性肺损伤 (AL I)及多器官功能障碍综合征 (MODS)的治疗效应及可能机制。方法 :采用家兔创伤性 AL I模型 ,实验动物随机分为正常对照组 (8只 )、创伤性 AL I组 (8只 )和丹参治疗组(8只 ) ,进行各组动物动脉血气 ,血浆和支气管肺泡灌洗液 (BAL F)中肿瘤坏死因子 α(TNFα)含量及 BAL F中白细胞数量、补体 C3a、C5 a、白蛋白含量的测定。用免疫组织化学结合原位定量分析方法检测肺、肝、心、肾组织 TNFα蛋白表达、分布及相对含量 ,并进行各组织的病理学光镜检查。结果 :丹参能改善创伤性 AL I动物的血气 ,不同程度降低外周血 TNFα及 BAL F中 TNFα、C3a、C5 a和白蛋白含量 ,抑制肺、肝、心、肾组织中TNFα的蛋白表达 ,减轻内脏组织的损伤程度。结论 :丹参能减少组织及血浆 TNFα的生成及含量 ,降低TNFα等细胞因子介导的多器官组织损害 ,在一定程度上缓解 AL I和 MODS的发生。
Objective:To study the preventive and therapeutic effects of Radix Salviae Miltiorrhizae on posttraumatic acute lung injury (ALI) and multiple organ dysfunction syndrome (MODS).Methods:Rabbit model of traumatic ALI was used in this study.Rabbits were randomly divided into the normal control group (group C,n=8),ALI group (group M,n=8) and Radix Salviae Miltiorrhizae treatment group (group T, n=8 ).The effects of Radix Salviae Miltiorrhizae on arterial blood gas,contents of tumor necrosis factorα( TNFα ) in plasma and bronchoalveolar lavage fluid (BALF),and neutrophils counts,and the contents of albumin,C3a,C5a in BALF were analyzed.By using immunohistochemistry combined with in situ quantitative analysis,the distribution and relative contents of TNFα in lung,liver,heart and kidney were determined.The pathological changes were examined with light microscope in various tissues.Results:Radix Salviae Miltiorrhizae could significantly improve the blood gas status,decrease the plasma level of TNFα and tissue contents of TNFα,albumin,C3a and C5a in BALF and lower the expression of TNFα in lung,liver,heart and kidney,thus ameliorating impairment of functions of visceral organs in traumatic ALI rabbits.Conclusions:Radix Salviae Miltiorrhizae can decrease the severity of organ damages in visceral organs and the incidence of ALI and MODS,possibly through the inhibition of the expression of TNFα in these tissues.
出处
《中国危重病急救医学》
CAS
CSCD
2000年第9期515-518,共4页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目!(39770736)
关键词
肺损伤
创伤性
TNF-Α
中医药疗法
trauma
acute lung injury
Radix Salviae Miltiorrhizae
tumor necrosis factor-α
