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目的探讨精氨酸酶抑制剂nor-NOHA对自发性高血压大鼠(SHR)血管重构的影响。方法WKY大鼠作为对照组,SHR随机分为模型组与受试组,受试组每天腹腔注射nor-NOHA(40mg/kg),定期测量大鼠收缩压和体质量,10周后,采用酶谱法检测心、肾及胸主动脉组织中活性MMP-2的含量,并对胸主动脉进行Tricrome-Masson,Picric-Siriusred及Orcein组织特染观察中膜厚度(MT)、管腔内径(LD)、径腔比(M/L)、Ⅰ型和Ⅲ型胶原及弹力纤维面积百分比值等。结果受试组收缩压显著下降、左心室MMP-2较SHR组含量显著降低(P<0.05),胸主动脉的MT、M/L、Ⅰ型和Ⅲ型胶原蛋白均下降(P<0.05)。结论nor-NOHA可能通过抑制MMP-2活性及降低Ⅰ型和Ⅲ型胶原的合成而缓解SHR血管重构。
Objective To investigate the effect of arginase inhibitor nor-NOHA on vascular remodeling in spontaneously hypertensive rats (SHR). Methods WKY rats were used as control group. SHR rats were randomly divided into model group and test group. The rats in test group were given intraperitoneal injection of nor-NOHA (40 mg / kg) daily. Systolic pressure and body weight were measured regularly. After 10 weeks, The content of active MMP-2 in heart, kidney and thoracic aorta was detected by spectrometry. The thoracic aorta was examined by Tricrome-Masson, Picric-Siriusred and Orcein Tissue Staining. ), Lumen ratio (M / L), type Ⅰ and type Ⅲ collagen and elastic fiber area percentage value. Results Compared with the SHR group, the content of MMP-2 in the left ventricle was significantly decreased (P <0.05), and the contents of MT, M / L, type I and type III collagen in the thoracic aorta decreased . Conclusion NO-NOHA may relieve the remodeling of SHR by inhibiting the activity of MMP-2 and decreasing the synthesis of type I and III collagen.