中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2010年
17期
3148-3152
,共5页
高虹%董少红%曾春苗%罗特丹%刘华东
高虹%董少紅%曾春苗%囉特丹%劉華東
고홍%동소홍%증춘묘%라특단%류화동
瑞舒伐他汀%颈动脉狭窄%疾病模型%动物%球囊%血管损伤%支架置入
瑞舒伐他汀%頸動脈狹窄%疾病模型%動物%毬囊%血管損傷%支架置入
서서벌타정%경동맥협착%질병모형%동물%구낭%혈관손상%지가치입
背景:球囊扩张及支架置入后再狭窄、管腔丢失等问题制约了支架置入治疗的进一步发展,血管内膜增殖和凋亡在再狭窄中的作用及干预方法尚在积极探索中.目的:采用Medtronic球囊建立大鼠颈动脉球囊损伤模型,观察瑞舒伐他汀对球囊损伤大鼠颈动脉平滑肌细胞增殖及凋亡的影响.方法:将雄性SD大鼠随机数字表法分为球囊损伤组和治疗组.均采用Medtronic球囊建立大鼠颈动脉球囊损伤模型,并取球囊损伤组大鼠的右侧颈总动脉(未行球囊损伤)作为正常对照.治疗组于球囊损伤前3 d始连续给予瑞舒伐他汀5 mg/(kg·d)灌胃,球囊损伤组给予9 g/L氯化钠溶液灌胃.术后7,14 d取颈总动脉进行苏木精-伊红染色,免疫组织化学检测SM α-actin、增殖细胞核抗原,采用TUNEL法检测平滑肌细胞凋亡情况.结果与结论:与球囊损伤组比较,治疗组造模后14 d,损伤血管新生内膜面积、新生内膜,中膜面积比值明显减少(P<0.05),管腔面积增加26%;增殖细胞核抗原阳性细胞率降低,凋亡阳性细胞率增高(P<o.05).提示支架置入球囊损伤前给予瑞舒伐他汀可抑制大鼠颈动脉球囊损伤后新生内膜增生及新生内膜细胞的增殖,促进平滑肌细胞的凋亡,从而减少动脉新生内膜形成,抑制再狭窄.
揹景:毬囊擴張及支架置入後再狹窄、管腔丟失等問題製約瞭支架置入治療的進一步髮展,血管內膜增殖和凋亡在再狹窄中的作用及榦預方法尚在積極探索中.目的:採用Medtronic毬囊建立大鼠頸動脈毬囊損傷模型,觀察瑞舒伐他汀對毬囊損傷大鼠頸動脈平滑肌細胞增殖及凋亡的影響.方法:將雄性SD大鼠隨機數字錶法分為毬囊損傷組和治療組.均採用Medtronic毬囊建立大鼠頸動脈毬囊損傷模型,併取毬囊損傷組大鼠的右側頸總動脈(未行毬囊損傷)作為正常對照.治療組于毬囊損傷前3 d始連續給予瑞舒伐他汀5 mg/(kg·d)灌胃,毬囊損傷組給予9 g/L氯化鈉溶液灌胃.術後7,14 d取頸總動脈進行囌木精-伊紅染色,免疫組織化學檢測SM α-actin、增殖細胞覈抗原,採用TUNEL法檢測平滑肌細胞凋亡情況.結果與結論:與毬囊損傷組比較,治療組造模後14 d,損傷血管新生內膜麵積、新生內膜,中膜麵積比值明顯減少(P<0.05),管腔麵積增加26%;增殖細胞覈抗原暘性細胞率降低,凋亡暘性細胞率增高(P<o.05).提示支架置入毬囊損傷前給予瑞舒伐他汀可抑製大鼠頸動脈毬囊損傷後新生內膜增生及新生內膜細胞的增殖,促進平滑肌細胞的凋亡,從而減少動脈新生內膜形成,抑製再狹窄.
배경:구낭확장급지가치입후재협착、관강주실등문제제약료지가치입치료적진일보발전,혈관내막증식화조망재재협착중적작용급간예방법상재적겁탐색중.목적:채용Medtronic구낭건립대서경동맥구낭손상모형,관찰서서벌타정대구낭손상대서경동맥평활기세포증식급조망적영향.방법:장웅성SD대서수궤수자표법분위구낭손상조화치료조.균채용Medtronic구낭건립대서경동맥구낭손상모형,병취구낭손상조대서적우측경총동맥(미행구낭손상)작위정상대조.치료조우구낭손상전3 d시련속급여서서벌타정5 mg/(kg·d)관위,구낭손상조급여9 g/L록화납용액관위.술후7,14 d취경총동맥진행소목정-이홍염색,면역조직화학검측SM α-actin、증식세포핵항원,채용TUNEL법검측평활기세포조망정황.결과여결론:여구낭손상조비교,치료조조모후14 d,손상혈관신생내막면적、신생내막,중막면적비치명현감소(P<0.05),관강면적증가26%;증식세포핵항원양성세포솔강저,조망양성세포솔증고(P<o.05).제시지가치입구낭손상전급여서서벌타정가억제대서경동맥구낭손상후신생내막증생급신생내막세포적증식,촉진평활기세포적조망,종이감소동맥신생내막형성,억제재협착.
BACKGROUND:Restenosis and lumina loss limit further application of balloon extension and stent implantation.Effect of tunica intima proliferation and apoptosis in restenosis and the intervention method are exploring.OBJECTIVE:To investigate the influence of Rosuvastatin on the vascular smooth muscle cells proliferation and apoptosis in rats with carotid artery injury established by Medtronic balloon.METHODS:The male SD rats were randomly and equally divided into injury group and treatment group.Each rat was subjected to balloon injury on the lift common carotid artery,and control artery without balloon injury on the right artery served as control group.Treatment group rats were given Rosuvastatin(dissolved in Nacl)5 mg/kg per day 3 days before injury,while the injury group rats were given 9 g/L NaCl.At 7 and 14 days after injury,the common carotid arteries were harvested for HE staining.SM α-actin and proliferating celI nuclear antigen were detected by immunohistochemistry.In addition,smooth muscle cells apoptosis was detected by TUNEL.RESULTS AND CONCLUSION:The neointimal area and the area ratio of neointimal/media were decreased in treatment grouP significantly at 14 days compared with injury group(P<0.05),and neointimal area increased by 26%:positive cell rate of proliferating cell nuclear antigen was decreased,but apoptosis cells were increased cornpared with the injury group(P<0.05).Results showed that Rosuvastatin prior to balloon injury inhibited neointimal proliferation and neointimal celI proliferation following balloon Injury,promoted smooth muscle cells apoptosis,ultimately reducing neointimaI formation and inhibiting restenosis.