摘要
背景:对慢性软组织损伤后一氧化氮合酶系统和一氧化氮的研究目前较少。目的:观察青白散对大鼠慢性软组织损伤模型骨骼肌中一氧化氮合酶系统和一氧化氮的影响。方法:雄性SD大鼠随机分为对照组、模型组、氨基胍组、青白散组。后3组采用机械损伤法制备慢性骨骼肌损伤动物模型,分别予以生理盐水10mL/kg,0.10g/kg氨基胍,0.54g/kg青白散,1次/d,连续14d。于给药后1,2,3周,分别检测大鼠肌组织一氧化氮含量、总一氧化氮合酶和诱导型一氧化氮合酶的活性。结果与结论:骨骼肌损伤修复过程中,模型组大鼠骨骼肌中一氧化氮含量、总一氧化氮合酶和诱导型一氧化氮合酶的活性较对照组显著增高;而青白散组和氨基胍组大鼠骨骼肌中一氧化氮含量、总一氧化氮合酶和诱导型一氧化氮合酶的活性均较模型组显著降低。说明青白散可能通过阻抑诱导型一氧化氮合酶诱导过量一氧化氮的产生,为慢性软组织损伤的修复创造了有利条件。
BACKGROUND：There have been few studies describing nitric oxide synthase （NOS） system and nitric oxide （NO） expression after chronic soft tissue injury. OBJECTIVE：To observe the effect of Qingbai powder on NOS system and NO in rat skeletal muscle of chronic muscle injury model. METHODS：Seventy two male SD rats were randomly and equally divided into four groups：control, model, aminoguanidine, Qingbai powder. Rats from the latter three groups were developed into model of chronic skeletal muscle injury by mechanical injury methods and then given 10 mL/kg normal saline, 0.10 g/kg aminoguanidine, 0.54 g/kg Qingbai power respectively, once a day, for successive 14 days. At 1, 2, and 3 weeks after administration, NO content, total NOS and inducible NOS activity in rat skeletal muscle tissue were detected. RESULTS AND CONCLUSION：During skeletal muscle healing process, NO content and total NOS and inducible NOS activity in rat skeletal muscle were significantly greater in the model group than in the control group. However, these indices were significantly lower in the Qingbai powder and aminoguanidine groups than in the model group. Results showed that Qingbai powder can induce the excessive production of NO by inhibiting inducible NOS, which creates favorable conditions for the recovery of chronic soft tissue injury.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2011年第37期6963-6966,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research
基金
成都体育学院博士建设期专项基金资助(编号BSZX1051)~~
