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组织缺血-再灌注激活全身性炎性反应引起严重急性肺损伤,其发病机理包含中性粒细胞激活及氧自由基产生。本研究检验的Butyrolactone抗炎剂FL1003具有体外抗氧化性,能下调这种炎性反应及消除急性肺损伤。雄性鼠共16只分三组:组1为假手术对照组(n=4),不予堵断血流;组2为缺血-再灌注组(n=7),肾动脉下端堵断2h随后再灌注1h,不使用药物治疗;组3为损伤治疗组(n=5),组织缺
Tissue ischemia-reperfusion activates systemic inflammatory response to cause severe acute lung injury, whose pathogenesis includes neutrophil activation and oxygen free radical production. This study examined the Butyrolactone anti-inflammatory agent FL1003 in vitro antioxidant activity, can down-regulate this inflammatory response and eliminate acute lung injury. A total of 16 male rats were divided into three groups: Group 1 was a sham operation control group (n = 4), blood flow was not blocked; Group 2 was ischemia-reperfusion group (n = 7) Followed by reperfusion 1h, without drug treatment; group 3 for the injury treatment group (n = 5), lack of tissue