Aim To investigate the protective role of salvianolic acid B ( Sal B ) on cardiac hypertrophy in type 2 diabetes mice , and to explore its influence on peroxisome proliferator activated receptors-α( PPARα) .Methods The type 2 diabetes melitus ( T2DM) mouse model was established by 4 weeks ' high fat diets feeding and one time STZ intraperitoneal injection .The animals were randomly divided into:control, T2DM, T2DM+SalB(100 mg· kg -1 · d-1 ) and Sal B(100 mg· kg -1 · d-1 ) groups.Eight weeks later, heart weight, tibial length, cross section area of cardiomyocytes , protein expression of PPARαin heart tissue were recorded .In vitro, high glucose and high insulin ( HGI ) were used to induce hypertrophic growth in cultured neonatal rat cardiomyocytes ( NRC-Ms) .And cell surface area , 3 H-leucine incorporation , 3 H-D-glucose uptake and PPARαprotein level were measured to observe the effect of Sal B and MK 886, a PPARαinhibitor.Results In T2DM model mice, Sal B could lower heart weight/tibial length and cross sec-tion area of cardiomyocytes , while PPARαprotein level in hearts were improved .In cultured cardiomyocytes , Sal B ( 10 ～100 μmol · L-1 ) ameliorated the in-creased levels of cell surface area ,3 H-leucine incorpo-ration and improved the decreased 3 H-D-glucose up-take and PPARαexpression induced by HGI . But those function could be abolished by MK 886.Conclu-sion Sal B ameliorates cardiac hypertrophy in T 2DM mice, which may be related to its function on PPARαactivation .%目的 研究丹酚酸B(Sal B)对2型糖尿病(T2DM)模型小鼠心肌肥厚的影响,并从过氧化物酶体增殖物激活受体α(PPARα)角度探讨其机制.方法 采用高脂饮食喂养4周联合链脲佐菌素(streptozotocin,STZ)单次腹腔注射法建立T2DM小鼠模型,实验小鼠分为对照组(control)、T2DM模型组、T2DM+Sal B组、Sal B组,上述条件继续饲养8周.检测各组小鼠心脏重量、胫骨长度、心肌细胞横截面积及心脏PPARα表达水平.体外采用高糖联合高胰岛素(HGI)诱导乳大鼠心肌细胞肥大,观察Sal B及PPARα抑制剂MK886对心肌细胞表面积、3H-亮氨酸参入率、3H-D-葡萄糖参入率及PPARα表达的影响.结果 Sal B能降低T2 DM模型小鼠心脏重量/胫骨长度比例、心肌细胞横截面积,并上调心脏组织PPARα表达水平.体外Sal B(10-100μmol·L-1)能浓度依赖性地抑制HGI诱导的心肌细胞表面积、亮氨酸参入率增加及3 H-D-葡萄糖参入率、PPARα的下调,但上述效应能够被MK886所消除.结论 Sal B能够抑制T2DM模型小鼠的心肌肥厚,其机制与上调PPARα表达有关.
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