中华外科杂志
中華外科雜誌
중화외과잡지
CHINESE JOURNAL OF SURGERY
2012年
10期
923-927
,共5页
商弢%刘昭%周敏%刘长建
商弢%劉昭%週敏%劉長建
상도%류소%주민%류장건
主动脉瘤,腹%丹参酮%基质金属蛋白酶2%基质金属蛋白酶9%趋化因子CCL2%一氧化氮合酶
主動脈瘤,腹%丹參酮%基質金屬蛋白酶2%基質金屬蛋白酶9%趨化因子CCL2%一氧化氮閤酶
주동맥류,복%단삼동%기질금속단백매2%기질금속단백매9%추화인자CCL2%일양화담합매
Aortic aneurysm,abdominal%Tanshinone%Matrix metalloproteinase2%Matrix metalloproteinase 9%Chemokine CCL2%Nitric oxide synthase
目的 研究丹参酮ⅡA对实验性大鼠腹主动脉瘤的抑制作用.方法 SD雄性大鼠36只随机平均分成实验组、对照组、空白组.实验组与对照组予胰弹力蛋白酶灌注肾下段腹主动脉,空白组予生理盐水灌注.实验组全程腹腔内注射丹参酮ⅡA 2 mg/d,对照组与空白组予生理盐水腹腔内注射.术前和术后第5、12、18、24天使用多普勒超声测量动脉瘤最大处内径并测量动脉收缩压.术后24 d取腹主动脉观察组织学变化并通过免疫组化、Western blot法、RT-PCR方法进行分析.结果 术后24 d实验组腹主动脉瘤直径较对照组明显减小[(0.210±0.002) cm比(0.304±0.004) cm,t=78.858,P=0.000],但各组血压手术前后无明显变化(t=-1.237～ -1.221,P＞0.05).实验组标本弹性纤维含量明显高于对照组(0.469±0.040比0.230±0.024,t=17.944,P=0.000),管壁结构较完整保存.实验组基质金属蛋白酶(MMP)-2与MMP-9在mRNA转录和蛋白质表达水平上均较对照组明下降(t=25.943,P=0.000;t =42.815,P =0.000),同时单核细胞趋化蛋白1(MCP-1)与诱导型一氧化氮合酶( iNOS)表达则明显较对照组减少(t=4.518,P=0.000;t =17.685,P=0.000).结论 丹参酮ⅡA可通过下调MMP-2和MMP-9表达、抑制MCP-1及iNZS合成,显著抑制实验动物腹主动脉瘤的扩张.
目的 研究丹參酮ⅡA對實驗性大鼠腹主動脈瘤的抑製作用.方法 SD雄性大鼠36隻隨機平均分成實驗組、對照組、空白組.實驗組與對照組予胰彈力蛋白酶灌註腎下段腹主動脈,空白組予生理鹽水灌註.實驗組全程腹腔內註射丹參酮ⅡA 2 mg/d,對照組與空白組予生理鹽水腹腔內註射.術前和術後第5、12、18、24天使用多普勒超聲測量動脈瘤最大處內徑併測量動脈收縮壓.術後24 d取腹主動脈觀察組織學變化併通過免疫組化、Western blot法、RT-PCR方法進行分析.結果 術後24 d實驗組腹主動脈瘤直徑較對照組明顯減小[(0.210±0.002) cm比(0.304±0.004) cm,t=78.858,P=0.000],但各組血壓手術前後無明顯變化(t=-1.237～ -1.221,P＞0.05).實驗組標本彈性纖維含量明顯高于對照組(0.469±0.040比0.230±0.024,t=17.944,P=0.000),管壁結構較完整保存.實驗組基質金屬蛋白酶(MMP)-2與MMP-9在mRNA轉錄和蛋白質錶達水平上均較對照組明下降(t=25.943,P=0.000;t =42.815,P =0.000),同時單覈細胞趨化蛋白1(MCP-1)與誘導型一氧化氮閤酶( iNOS)錶達則明顯較對照組減少(t=4.518,P=0.000;t =17.685,P=0.000).結論 丹參酮ⅡA可通過下調MMP-2和MMP-9錶達、抑製MCP-1及iNZS閤成,顯著抑製實驗動物腹主動脈瘤的擴張.
목적 연구단삼동ⅡA대실험성대서복주동맥류적억제작용.방법 SD웅성대서36지수궤평균분성실험조、대조조、공백조.실험조여대조조여이탄력단백매관주신하단복주동맥,공백조여생리염수관주.실험조전정복강내주사단삼동ⅡA 2 mg/d,대조조여공백조여생리염수복강내주사.술전화술후제5、12、18、24천사용다보륵초성측량동맥류최대처내경병측량동맥수축압.술후24 d취복주동맥관찰조직학변화병통과면역조화、Western blot법、RT-PCR방법진행분석.결과 술후24 d실험조복주동맥류직경교대조조명현감소[(0.210±0.002) cm비(0.304±0.004) cm,t=78.858,P=0.000],단각조혈압수술전후무명현변화(t=-1.237～ -1.221,P＞0.05).실험조표본탄성섬유함량명현고우대조조(0.469±0.040비0.230±0.024,t=17.944,P=0.000),관벽결구교완정보존.실험조기질금속단백매(MMP)-2여MMP-9재mRNA전록화단백질표체수평상균교대조조명하강(t=25.943,P=0.000;t =42.815,P =0.000),동시단핵세포추화단백1(MCP-1)여유도형일양화담합매( iNOS)표체칙명현교대조조감소(t=4.518,P=0.000;t =17.685,P=0.000).결론 단삼동ⅡA가통과하조MMP-2화MMP-9표체、억제MCP-1급iNZS합성,현저억제실험동물복주동맥류적확장.
Objective To determine if tanshinone Ⅱ A (Tan Ⅱ A) can influence the development of elastase-induced experimental abdominal aortic aneurysms (AAAs).Methods Totally 36 male SpragueDawley rats were randomly distributed into three groups ( 12 in each group):Tan Ⅱ A group,control group,and sham group. Rats of Tan Ⅱ A and control groups underwent intra-aortic elastase perfusion to induce AAAs,while rats of sham-group were perfused with saline. Rats of Tan Ⅱ A-group received Tan Ⅱ A treatment (2 mg/d).The luminal diameter of the aneurysm at the segment with maximum diameter were measured pre-perfusion and on the 4 time point after perfusion.Systolic blood pressure was measured by tailcuff technique.Aortic tissue samples were obtained on 24 days after perfusion and evaluated by RT-PCR,Western blot,immunohistochemistry and Miller's elastin-Van Gieson's (EVG) staining.Results Twentyfour days after perfusion,Tan Ⅱ A significantly reduced increased aortic size compared to control group ( (0.210 ±0.002) cm vs.(0.304 ±0.004) cm,t =78.858,P =0.000) without affecting blood pressure (t =- 1.237 to - 1.221,P ＞0.05).The over-expression of matrix metalloproteinases ( MMP)-2/9 (t =25.943,P =0.000; t =42.815,P =0.000),monocyte chemotactic protein-1 ( MCP-1 ) (t =4.518,P =0.000),inducible nitric oxide synthase (iNOS) (t =17.685,P =0.000) and the destruction of elastic fibers in aortic tissue of control group were significantly less than Tan Ⅱ A group (0.469 ± 0.040 vs.0.230 ± 0.024,t =17.944,P =0.000 ).Conclusion Tanshinone Ⅱ A attenuates the development of elastase-induced experimental AAAs possibly by down-regulating MMP-2/9,MCP-1 and iNOS expression.
