摘要
目的探讨基质金属蛋白酶(MMP1和MMP2)和内源性基质金属蛋白酶组织抑制因子(TIMP2)的活性变化在雄附方干预大鼠肺间质纤维化形成机制中的可能作用。方法 70只SD健康大鼠随机分为对照组(BC)、假手术组(PS)、纤维化模型组(MD)、醋酸泼尼松组(PN 5.6 mg/kg)、雄附方高、中、低剂量组(XFFH、XFFM和XFFL 1.4 g/kg、0.7 g/kg、0.35 g/kg)7组,每组10只。于造模后第2天用0.9%氯化钠注射液(0.014 L/kg)或相应药物(0.014 L/kg)每天灌胃(ig),4周后取右肺中叶组织,应用免疫组织化学染色(SP)法检测肺组织中MMP1、MMP2和TIMP2的表达水平。结果 MMP1、MMP2和TIMP2在MD组阳性表达水平均为各组最高(P<0.01);用药组中XFFH组MMP1、MMP2和TIMP2的阳性表达水平均最低(P<0.01);XFFH组与BC和PS组相比TIMP2表达增强(P<0.05)。结论雄附方对抗肺组织纤维化的形成机制可能与其有效平衡肺组织中MMP1、MMP2和TIMP2的表达水平有关。
Objective To study the role of MMP1,MMP2 and TIMP2 in treatment of pulmonary interstitial fibrosis in rats with Xiongfufang and its mechanism.Methods Seventy healthy SD rats were randomly divided into control group,sham operation group,fibrosis model group,prednione acetate group,and high,medium,low Xiongfufang dose groups（10 in each group）.On day 2 after a model was established,the rats were given 0.9% sodium chlorate or gastric drugs for 4 weeks.Expressions of MMP1,MMP2 and TIMP2 in lung tissue were detected with SP staining.Results The expression levels of MMP1,MMP2 and TIMP2 were significantly higher in fibrosis model group than in different drug treatment groups（P 0.01）.The expression level of TIMP2 was significantly higher in high Xiongfufang dose group than in control group and sham operation group（P 0.05）.Conclusion Xiongfufang prevents lungs against their interstitial fibrosis possibly by regulating the expression of MMP1,MMP2,and TIMP2 in lung tissue.
出处
《解放军医学院学报》
CAS
2013年第4期376-378,381,共4页
Academic Journal of Chinese PLA Medical School
基金
"十一五"军队中医药重大临床攻关课题(2006011003)
河北省2010年科技支撑计划项目(102761101)
河北省中医药管理局科学技术研究课题(2008071)
河北大学博士基金(2011213)
