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作 者:林红[1]
机构地区:[1]江苏省连云港市中医院,江苏连云港222000
出 处:《中国药师》2016年第5期836-838,共3页China Pharmacist
摘 要: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 study the protective effect and possible mechanism of salvianolic acid B in GK rats complicated with macroangiopathy.Methods:Totally 32 GK rats were randomly divided into four groups:the model group and low,middle and high dose salvianolic acid B groups(40,80 and 160 mg·kg^-1),and 8 Wistar rats were used as the normal group.All of GK rats were given high-glucose and high-fat diet.After 16 weeks,GK rats were orally administrated with 10 mg · kg^-1·d^-1 N-ω-nitro-L-arginine methyl ester for 8 weeks.At the beginning and the end of the experiment,blood glucose and blood pressure were measured,abdominal aortic blood was collected after anesthesia,thoracic aorta was used to make paraffin sections after bloodletting to observe vasculopathy and the expression of VEGF was detected by Western-blot.Results:The blood glucose was increased in all GK rats with no statistical significance between the drug group and the model group(P〉0.05).At the end of the experiment,the blood pressure was significantly increased in GK rats,indicating that salvianolic acid B could notably reduce the blood pressure in GK rats in a dose-dependent manner with statistical significance(P〈0.05);and it could also remarkably reduce the total white blood cell count and differential blood count,and ameliorate the lesion extent and reduce VEGF expression.Conclusion:Salvianolic acid B has protective effects on aorta in GK rats,and its mechanism may be related with blood pressure lowering,anti-inflammation and reduction of VEGF expression.
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