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Tanshinone Ⅱ A attenuates the development of elastase-induced abdominal aortic aneurysm of rat

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Author:
No author available
Journal Title:
Chinese Journal of Surgery
Issue:
10
DOI:
10.3760/cma.j.issn.0529-5815.2012.10.014
Key Word:
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;Aortic aneurysm,abdominal;Tanshinone;Matrix metalloproteinase2;Matrix metalloproteinase 9;Chemokine CCL2;Nitric oxide synthase

Abstract: 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.

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