| Objective To investigate the characteristic and mechanism of vascular remodeling in spontaneously hypertensive rats and effect of XueFuZhu Yu decoctionMethods Twenty week-old male SHR (n=42) and age-matched Wistar rats (n=6) were randomly devided into 4 groups.The control group before treatment (SHRc, six spontaneously hypertensive rats and six Wistar rats); the negative control group (SHRNs, n=12,fed with 0.9% sodium chloride for 8 weeks, 10ml/kg.d);the positive control group(SHRA,n=12,fed with amlodipine suspension 0.5mg/ml for 8 weeks, 3.4ml/kg.d ); the treated group ( SHRA+x, n =12, fed with XueFuZhuYu decoction 10ml/kg.d, containing herbal drug 4.05g/ml and amlodipine suspension 3.4ml/kg.d for 8 weeks). After taking all rats blood pressure, the thoracic aorta of the control group before treatment were taken out and embeded the section with olefin. The specimens were stained so as to reveal the smooth muscle by alkalescence solferino and smooth muscle cell karyon by Harris and eosin seperately. Morphological changes was observed through optics microscope and the remodeling of inner diameter (ID), out diameter (OD), wall thickness (WT), wall thickness / inner diameter (WT/ID), corss-sectional area (CSA), the relative area of smooth muscle, and the amount of media smooth muscle cell karyon pressing close to vascular intima within 10 10 field of vision were analyzed by computerimage system and morphological quantitive method. RT-PCR (reverse trans-cription-polymerase chain reaction) technique was applied to detect the expression of ET-1 (endothelin -1), laminin and MMP-3 (matrix metal opro-teinase-3) gene in the thoracic aorta.Having been fed for 8 weeks, rats of SHRNs, SHRA, SHRA+x were received the same detection.Results Before treatment: (T) Blood pressure of SHR was higher signifycantly than that of Wistar rats. The OD,ID,WT, WT /ID,CSA and the relative area of smooth muscle were all increased compared with Wistar rats, especially for wall thickness( P<0.001).In the same size visual field the amount of VSMC karyon in SHR was less than that of Wistar rats significantly (P<0.001). (2)Under the endothelium of SHR thoracic aorta there were some foam cell from monocyte, synthetic phenotype smooth muscle cell and calcification. The amount of smooth muscle cell kayron closing to vascular intima augmented significantly.(3)ET-l mRNA, MMP-3 mRNA relative expression levels of SHR thoracic aorta were high significantly and laminin mRNA relative expression levels was lower significantly than that of WISTAR rats (P<0.01).After treatment:(1)Blood pressure of SHRA and SHRA+x declined significantly compared with that of SHRc and SHRNS CP<0.001). (2)The vascular WT of SHRNs was thicker significantly than that of SHRc (P<0.01)and SHRA,SHRA+x was thinner than that of SHRNsCP<0.05).(3)There was no obvious changes on microstructure components and atherosclerosis of SHR thoracic aorta.(4)As compared with SHRc, thoracic aorta ET-lmRNA, MMP-3mRNA relative expression levels of SHRns were higher (P<0.01,P<0.05) and laminin mRNA relative expression levels was lower (P<0.05) and SHRA, SHRA+x had no difference (P>0.05). On the contrary, as compared with SHRNS, thoracic aorta ET-1 mRNA, MMP-3 mRNA relative expression levels of SHRA and SHRA+X were decreased (P<0.01,/><0.05) and laminin mRNA relative expression levels was increased (P<0.01,P<0.05). Furthermore, ET-1 mRNA, MMP -3 mRNA relative expression levels of SHRA+x was lower and laminin mRNA relative expression levels was higher than that of SHRA(P<0.05).Conclusion (1)High vascular luman pressure because of hypertension leads to thoracic aorta wall thicken, smooth muscle accumulated and vascular smooth muscle cell (VSMC) hypertrophy. High blood perssure can damnify vascular endothelium and results in vascular permeability increasing, which is the reason to induce the atherosclerosis happened with the normal blood lipid level. At the same time,endothelium cell secrete ET-1 that accelerates VSMC proliferation and monocyte infiltrate and activate MMP-3 which can...
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