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目的:探讨丹酚酸B对自发性糖尿病(GK)大鼠合并大血管病变的保护作用及可能的机制。方法:将32只GK大鼠随机分为模型组和丹酚酸B低、中、高剂量组(40,80,160 mg·kg~(-1)),另选取正常8只Wistar大鼠作为正常对照组。所有GK大鼠给予高糖、高脂饲料16周后以L-N-硝基甲酯(L-NAME)10 mg·kg~(-1)·d~(-1)灌胃,连续8周。给药开始及结束前对大鼠的血糖和血压进行检测,麻醉后取腹主动脉血进行血常规检测,放血后取胸主动脉制作病理切片,观察血管病变,Western-blot法检测血管内皮细胞生长因子(VEGF)的表达。结果:所有GK大鼠血糖水平持续升高,但模型组与给药组差异无统计学意义(P>0.05),模型组大鼠实验结束时血压显著升高,给予丹酚酸B可剂量依赖性降低血压,差异有统计学意义(P<0.05);丹酚酸B可显著降低模型大鼠的白细胞总数和分类计数,明显减轻血管病变程度并减少VEGF的表达。结论:丹酚酸B对自发性糖尿病大鼠的大血管具有明显的保护作用,其可能的机制为降低血压、抗炎以及降低VEGF的表达。
Objective: To investigate the protective effect of salvianolic acid B on spontaneously diabetic (GK) rats with macrovascular complications and its possible mechanism. Methods: Thirty-two GK rats were randomly divided into model group and low, medium and high dose salvianolic acid group (40, 80, 160 mg · kg -1), and another 8 normal Wistar rats were selected as normal control group. All GK rats were given high glucose and high fat diet for 16 weeks and then fed with L-NAME 10 mg · kg -1 d -1 for 8 weeks. Blood glucose and blood pressure were measured before and at the end of the administration. Blood samples were obtained from the abdominal aorta after anesthesia. Blood samples were obtained from the thoracic aorta after bloodletting. Pathological changes were observed. The vascular endothelial cells Growth factor (VEGF) expression. Results: The blood glucose level of all GK rats continued to increase, but there was no significant difference between the model group and the administration group (P> 0.05). In the model group, the blood pressure was significantly increased at the end of the experiment, and salvianolic acid B was dose-dependent (P <0.05). Salvianolic acid B could significantly reduce the total number of leucocytes and the number of leukocytes in model rats, significantly reduce the degree of vascular lesions and decrease the expression of VEGF. CONCLUSION: Salvianolic acid B has a significant protective effect on the large blood vessels in spontaneously diabetic rats. Its possible mechanism is to reduce blood pressure, anti-inflammation and decrease the expression of VEGF.