BACKGROUND Platelets in patients with type 2 diabetes mellitus (DM2) are characterized by increased activation and aggregation, which tends to be associated with a high morbidity and mortality due to cardiovascular disease (CVD). Moreover, a large proportion of DM2 patients show an inadequate response to standard antiplatelet treatments, contributing to recurrent cardiovascular events. In our previous study, we indicated that Salvianolic acid A (SAA) presents an antiplatelet effect in healthy volunteers. However, whether it can inhibit "activated platelets" with a pathologic status has not been explored. Therefore, this study was designed to investigate the antiplatelet effect of SAA and its diabetic complication-related difference in DM2. METHODS Forty patients diagnosed with DM2 from January 2018 to April 2018 were recruited. Fibrinogen-binding (PAC-1) and P-selectin (CD62p) flow cytometry reagents were measured under resting and stimulated conditions by flow cytometry, while agonist-induced platelet aggregation was conducted by light transmission aggregometry. Before all these measurements were conducted, all platelet samples were preincubated with a vehicle or SAA for 10 min. Additionally, the diabetic complication-related difference in the antiplatelet effect of SAA was further studied in enrolled patients. RESULTS The expressions of PAC-1 and CD62p were elevated in DM2, as well as the maximal platelet aggregation. In addition, SAA decreased the expressions of PAC-1 and CD62p, which were enhanced by ADP and thrombin (all P < 0.01). It also reduced the platelet aggregation induced by ADP (P < 0.001) and thrombin (P < 0.05). Comparing the antiplatelet effect of SAA on DM2, with and without diabetic complications, no statistically significant difference was found (all P > 0.05). CONCLUSIONS The present study demonstrated that SAA can inhibit platelet activation and aggregation in patients with DM2, and the inhibition did not abate for the existence of diabetic complications.

中文翻译：

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丹酚酸a抑制2型糖尿病患者的血小板活化和聚集。

背景技术2型糖尿病（DM2）患者的血小板的特征在于增加的活化和聚集，这倾向于与由于心血管疾病（CVD）引起的高发病率和高死亡率相关。此外，很大一部分的DM2患者对标准的抗血小板治疗反应不佳，导致心血管事件反复发作。在我们先前的研究中，我们表明丹酚酸A（SAA）对健康志愿者具有抗血小板作用。然而，尚未探讨其是否可以抑制具有病理状态的“活化血小板”。因此，本研究旨在研究SAA的抗血小板作用及其在DM2中与糖尿病并发症相关的差异。方法招募了2018年1月至2018年4月诊断为DM2的40例患者。纤维蛋白原结合（PAC-1）和P选择素（CD62p）流式细胞仪试剂在静止和刺激条件下通过流式细胞仪进行测定，而激动剂诱导的血小板聚集则通过光透射聚集法进行。在进行所有这些测量之前，将所有血小板样品与溶媒或SAA预孵育10分钟。此外，在入组患者中还进一步研究了糖尿病并发症相关SAA抗血小板作用的差异。结果在DM2中，PAC-1和CD62p的表达升高，并且血小板聚集最大。此外，SAA降低了PAC-1和CD62p的表达，而ADP和凝血酶增强了PAC-1和CD62p的表达（所有P <0.01）。它还减少了ADP（P <0.001）和凝血酶（P <0.05）诱导的血小板聚集。比较SAA对DM2的抗血小板作用（有或没有糖尿病并发症），未发现统计学上的显着差异（所有P> 0.05）。结论本研究表明，SAA可以抑制DM2患者的血小板活化和聚集，并且这种抑制作用并不能减轻糖尿病并发症的存在。