摘要
目的研究在尾加压素Ⅱ(UⅡ)受体拮抗剂Urantide干预下,转化生长因子-β1(TGF-β1)在大鼠动脉粥样硬化(AS)胸主动脉中的表达情况,探讨在AS时TGF-β1与羟脯氨酸(HYP)之间的关系。方法采用高脂饲料喂养及腹腔注射VD3损伤动脉内膜的方法建立大鼠AS模型,随机分为4组:对照组、模型组、氟伐他汀组、Urantide组,生物化学方法检测血清及尿液中HYP含量;免疫组织化学法检测主动脉壁内TGF-β1的表达水平。结果 Urantide组血清中HYP在给药3 d后即明显低于模型对照组,7 d进一步降低,14 d时血清中HYP含量降低接近于阳性药对照组(P<0.01)。在胸主动脉内膜及中膜斑块内,Urantide各给药组TGF-β1阳性染色强度和范围较模型对照组明显增强(P<0.01)。结论随Urantide给药时间的增加,TGF-β1使动脉壁内的胶原蛋白分泌减少,缓解大鼠AS症状。
Objective To study the expression of tr ansforming growth factor-β(TGF-β1) in the atherosclerotic(AS) rat′s tho racic aorta under the intervention of Urantide,which is urotensin Ⅱ receptor a ntagonist and probe the relationship between the TGF-β1 and hydroxyproline( HYP) in AS. Methods AS model was induced by feeding high fat diet and arterial intimal injury of intraperitoneal injection of VD3.Rats were randomly divided into control,model,Fluvastatin,Urantide groups.The expression of HYP content was detected by biochemical me thod.The expression of TGF-β1 protein was detected by immunological histoc hemical method. Results Serum HYP in Urantide group at the administration of 3 days was s ignificantly lower than that of model group,further reduced at 7 days,close to that of positive drug control group at 14 days(P〈0.01).The positive st aining intensity and scope of TGF-β1 in each Urantide treatment groups were enhanced obviously comparing with model group(P〈0.01). Conclusions With the Urantide admi nistration time increasing,TGF-β1 causes hyposecretion of collagen in the arterial walls and the collagen in the serum is discharged with the urine in for m of HYP.Thus AS symptom of the rat is relieved.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2011年第24期4839-4841,共3页
Chinese Journal of Gerontology
基金
国家自然科学基金主任基金(81141045)
全国临床医药专项基金项目(L2011315)
吉林省科技厅重大项目资助课题(2005040425)