Lin Chiu-Mei, Wang Bao-Wei, Fang Wei-Jen, Pan Chun-Ming, Shyu Kou-Gi, Hou Sheng-Wen
Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
Faculty of Medicine, School of Medicine, Fu Jen Catholic University, Taipei, Taiwan.
Planta Med. 2019 Mar;85(5):406-411. doi: 10.1055/a-0818-3689. Epub 2019 Jan 4.
Catalpol, an iridoid glycoside, is an isolated natural product of , which has been reported to have antidiabetic properties. This study investigated the vascular protective effects of catalpol in hyperglycemic rats with balloon-injured carotid arteries. Balloon injury stress led to the upregulation of monocyte chemoattractant protein-1 expression in rats with streptozotocin-induced diabetes. Western blotting and real-time PCR were performed. hybridization, immunohistochemistry, and confocal analyses were employed. Monocyte chemoattractant protein-1 levels were increased through streptozotocin induction or balloon injury. After treatment with catalpol, the neointimal hyperplasia area was reduced 2 weeks after balloon injury in hyperglycemic rats. Real-time PCR and immunohistochemical analysis demonstrated reduced levels of monocyte chemoattractant protein-1 2 weeks after the balloon injury. Monocyte chemoattractant protein-1 expression was significantly increased in balloon-injured rats compared with the control groups. Thus, treatment with catalpol affected monocyte chemoattractant protein-1 expression. This study demonstrated that catalpol downregulated monocyte chemoattractant protein-1 expression in carotid arteries and ameliorated neointimal hyperplasia in hyperglycemic rats. The suppressive effect of monocyte chemoattractant protein-1 suggests that it plays a key role in neointimal hyperplasia. The results imply that catalpol is potentially effective for preventing hyperglycemia-related ischemic cardiac diseases.
梓醇是一种环烯醚萜苷,是从[具体来源未明确]中分离出的天然产物,据报道具有抗糖尿病特性。本研究调查了梓醇对颈动脉球囊损伤的高血糖大鼠的血管保护作用。球囊损伤应激导致链脲佐菌素诱导的糖尿病大鼠单核细胞趋化蛋白-1表达上调。进行了蛋白质免疫印迹法和实时定量聚合酶链反应。采用了[此处原文未明确具体技术,可能是某种杂交技术]杂交、免疫组织化学和共聚焦分析。单核细胞趋化蛋白-1水平通过链脲佐菌素诱导或球囊损伤而升高。用梓醇治疗后,高血糖大鼠球囊损伤2周后新生内膜增生面积减小。实时定量聚合酶链反应和免疫组织化学分析表明,球囊损伤2周后单核细胞趋化蛋白-1水平降低。与对照组相比,球囊损伤大鼠的单核细胞趋化蛋白-1表达显著增加。因此,梓醇治疗影响了单核细胞趋化蛋白-1的表达。本研究表明,梓醇下调颈动脉中单核细胞趋化蛋白-1的表达,并改善高血糖大鼠的新生内膜增生。单核细胞趋化蛋白-1的抑制作用表明其在新生内膜增生中起关键作用。结果表明梓醇对预防高血糖相关的缺血性心脏病可能有效。